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Hyun Kyung Lim, , , Jung Yin Huh, Ji Hwa Ryu, Jin Yong Sung, Sung Hee Park
Published: 16 October 2017
Endocrine Research, Volume 43, pp 65-72; https://doi.org/10.1080/07435800.2017.1381973

Abstract:
The effect of ultrasonography (US)-guided fine-needle aspiration (US-FNA) for the collapse of benign cystic thyroid nodules is still unclear. This study aimed to assess the positive response rate following US-FNA of the cystic component of thyroid cysts and of partially cystic thyroid nodules (PCTNs), and to evaluate the factors influencing the outcome.
Bianca Rudolphi, Benedikt Zapp, Nils A. Kraus, Franziska Ehebauer, Bettina J. Kraus,
Published: 16 October 2017
Endocrine Research, Volume 43, pp 55-63; https://doi.org/10.1080/07435800.2017.1381972

Abstract:
Nicotinamide N-methyltransferase (NNMT) is a novel regulator of energy homeostasis in adipose tissue. NNMT expression is higher in obese mice than in lean mice, and NNMT knockdown prevents diet-induced obesity. Little is known about the regulation of enzyme activity during the development of obesity. The aim of this study was to analyze NNMT activity in tissues of mice with incipient and established obesity.A fluorescence-based, sensitive, low-volume, high-throughput method was developed to assay NNMT activity. C57BL/6 mice were fed a high-fat diet for 4 weeks (incipient obesity) and for 12 weeks (established obesity). Tissues and serum were harvested and analyzed.NNMT activity was highest in subcutaneous white fat (55.0 µU/mg), followed by epididymal white fat (35.6 µU/mg), brown adipose tissue (7.8 µU/mg), liver (7.6 µU/mg), and lung (7.3 µU/mg). Little activity was detected in heart, skeletal muscle, and kidney. No activity was found in serum samples. Body weight predicted NNMT activity in white fat, but not in brown fat or any other tissue, and only in incipient obesity. With established obesity, this association was lost.As obesity develops, body weight predicts NNMT activity in white adipose tissue, but not in any other tissue, consistent with a specific role of adipose-tissue NNMT in the regulation of body weight.
, Eun-Jin Yang, ,
Published: 13 October 2017
Endocrine Research, Volume 43, pp 47-54; https://doi.org/10.1080/07435800.2017.1379023

Abstract:
Purpose: Metabolic syndrome increases the risk of cardiovascular disease. Recently glucagon-like peptide 1 (GLP-1) agonists proved to be effective in preventing cardiovascular disease (CVD) in patients with type 2 diabetes. We investigated the association of blood incretin levels with metabolic syndrome in patients with type 2 diabetes. Materials and methods: This is a cross-sectional study involving 334 people with type 2 diabetes. Intact GLP-1 (iGLP-1) and intact glucose-dependent insulinotropic polypeptide (iGIP) levels were measured in a fasted state and 30 min after ingestion of a standard mixed meal. Metabolic syndrome was diagnosed based on the criteria of the International Diabetes Federation. Results: Two hundred twenty-five (69%) of the subjects have metabolic syndrome. The fasting iGLP-1 level was no different between groups. Thirty-min postprandial iGLP-1 was non-significantly lower in the subjects who had metabolic syndrome. Incremental iGLP-1 (ΔiGLP-1, the difference between 30-min postmeal and fasting iGLP-1 levels) was significantly lower in those with metabolic syndrome. There were no significant differences in fasting iGIP, postprandial iGIP, and ΔiGIP between groups. The ΔiGLP-1, but not ΔiGIP levels decreased significantly as the number of metabolic syndrome components increased. In hierarchical logistic regression analysis, the ΔiGLP-1 level was found to be a significant contributor to metabolic syndrome even after adjusting for other covariates. Conclusion: Taken together, the iGLP-1 increment in the 30 min after meal ingestion is inversely associated with metabolic syndrome in patients with type 2 diabetes. This suggests that postmeal iGLP-1 increment could be useful in assessing cardiovascular risk in type 2 diabetes.
Published: 3 October 2017
Endocrine Research, Volume 43, pp 39-46; https://doi.org/10.1080/07435800.2017.1374967

Abstract:
Background: little is known on the influences of normal menstrual cycle on prolactin gene expression in immune cells. Aim of the study: to determine the effects of the ovarian cycle on prolactin and its receptor expression. Methods: peripheral blood mononuclear cells (PBMC) were obtained from twenty-six normal menstruating women at different intervals of their menstrual cycle. The PBMC were incubated during 24 h in the presence or absence of Concanavalin-A (Con-A) and the gene expression of PRL, PRLR and cytokines was evaluated by qPCR. Prolactin, IL-2 and cAMP were determined in each culture by specific immunoassays. Results: neither PRL nor its receptor expression in PBMC changed significantly among groups, including the cytokines (IL-2, IL-10, and IFNG) studied. Similar results, among groups, were obtained, when PRL expression was stimulated by PGE2 or 8-Br-cAMP. Concanavalin A-stimulated PBMC expressed significantly less prolactin and a significant negative correlation between secreted IL-2 and PRL expression was found. The presence of anti-IL-2 antibodies in Con-A stimulated-cultures significantly increased PRL expression when compared to control cells regardless the hormonal status. Conclusions: these data suggest that the menstrual cycle does not significantly modulate or influence prolactin and cytokines gene expression in PBMC, and indicate that IL-2 may be involved in the Con-A regulation of PRL expression in immune cells.
Na Wang, Peng Xue, Xuelun Wu, Jianxia Ma, Yan Wang,
Published: 3 October 2017
Endocrine Research, Volume 43, pp 29-38; https://doi.org/10.1080/07435800.2017.1373662

Abstract:
Purpose: This study aimed to investigate the role of sclerostin and dkk1 in the bone metabolism of type 2 diabetic patients. Methods: This cross-sectional study included 95 inpatients with type 2 diabetes mellitus. We divided the patients into three groups (i.e., the normal bone mineral density (BMD) group, osteopenia group and osteoporosis group) based on their different BMD levels and measured the serum levels of sclerostin, dkk1, 25-hydroxyvitamin D3 (25OHD3), bone turnover markers and other biochemical data in each group. Results: Significantly increased levels of serum sclerostin and dkk1 were found in the osteoporosis group, even when the male and female cohorts were considered separately. Ordinal logistic regression analysis suggested that the levels of serum sclerostin were independently associated with the presence of osteopenia and osteoporosis after adjusting for age, gender and 25OHD3 (sclerostin: OR = 1.02, p = 0.001). The areal BMDs were negatively correlated with the levels of serum sclerostin and dkk1 and positively correlated with 25OHD3. In addition, age, glycosylated hemoglobin and serum sclerostin levels were predictors for N-terminal propeptide of type 1 procollagen and serum dkk1 levels were the only predictors for crosslinked carboxyterminal telopeptide in type 1 collagen. Conclusions: The sclerostin and dkk1 levels increased in conjunction with the reduction of BMD, confirming that the Wnts, inhibited by sclerostin and dkk1, were potentially responsible for bone fragility in type 2 diabetes patients with osteoporosis. Note that the serum sclerostin levels were predictors for bone formation, while the DKK1 levels predicted bone resorption.
, Mustafa Caliskan, Muyesser Sayki Arslan, Taner Demirci, Suleyman Karakose, Esra Tutal, Erman Cakal
Published: 22 September 2017
Endocrine Research, Volume 43, pp 15-20; https://doi.org/10.1080/07435800.2017.1368543

Abstract:
Purpose: Primary hyperparathyroidism (PHPT) has been associated with increased incidence of morbidity and mortality of the cardiovascular system. The pathogenetic mechanisms underlying this association are still not completely clear. A disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS) play a critical role in atherosclerosis. This study aimed to investigate the levels of ADAMTS4 and ADAMTS9 and relationship between these proteoglycanases and cardiometabolic abnormalities in PHPT. Materials and Methods: A case-control study was performed in a training and research hospital. Fifty-six patients with PHPT and 61 healthy volunteers were recruited. The Framingham score was used to calculate cardiovascular risk (CVR). Serum ADAMTS levels were determined by a human enzyme-linked immunoassay in all subjects. Results: The ADAMTS9 concentration was significantly higher in patients with PHPT than in the control group (p< 0.05); however, there were no significant differences in ADAMTS4 levels between the groups (p > 0.05). In ROC curve analysis, PHPT can be predicted by the use of ADAMTS9 at a cut-off value of 30.7 pg/mL (69% sensitivity, 65% specificity). CVR score was significantly increased in the PHPT than controls (p< 0.05). ADAMTS4 and ADAMTS9 levels had positive correlations with CVR score (r = 0.322, p = 0.017; r = 0.275, p = 0.044 respectively). Conclusions: Based on the results of the present study, cardiovascular risk is increased in PHPT and associated with ADAMTS4 and ADAMTS9. Further efforts are needed to establish the function of ADAMTS proteases in both PHPT and atherosclerosis.
, M. James Lenhard, Ryan T. Pohlig, P. Babu Balagopal, Raafat Abdel-Misih
Published: 22 September 2017
Endocrine Research, Volume 43, pp 21-28; https://doi.org/10.1080/07435800.2017.1369432

Abstract:
Purpose: Surgical treatment for primary hyperparathyroidism (PHPT) improves bone metabolism. Osteocalcin (OC) and its undercarboxylated form (ucOC) are associated with bone and energy metabolism. Osteopontin (OPN), a multifunctional protein expressed in bone, is involved in resorption, along with β-carboxyl-terminal cross-linking telopeptide of type 1 collagen (β-CTX), and osteoprotegerin (OPG). Our aim was to investigate these biomarkers of bone metabolism in patients with PHPT. Methods: We examined 30 individuals with PHPT, in a clinical research facility, before and 1 month following parathyroidectomy. Circulating levels of OC, ucOC, OPN, β-CTX, and OPG were examined as bone biomarkers along with inflammatory markers (e.g., interleukin-6 [IL-6], lipocalin-2), insulin resistance (i.e., homeostasis model assessment for insulin resistance [HOMA-IR]), adiposity (i.e., leptin, adiponectin), PTH, calcium, 25-hydroxyvitamin D, creatinine, and demographics. Results: Participants (27 females/3 males) were 60 ± 9 (mean±SD) years old. There was a significant reduction of ucOC (7.9 ± 5.1 [median±SIQR] vs. 6.6 ± 3.7 ng/mL, p = 0.022) and OPN (75.4 ± 14.5 vs. 54.5 ± 9.2 ng/mL, p< 0.001) pre- versus post-parathyroidectomy. There were no univariate differences postoperatively for IL-6, HOMA-IR, leptin, or adiponectin. Regression analysis showed that postoperative levels of adiponectin, IL-6, and OPN were significantly associated with ucOC, while adjusting for PTH and albumin corrected calcium levels (model R2 = 0.610, p = 0.001). With OPN as the dependent variable, higher adiponectin and lower ucOC were significantly associated with lower OPN levels postoperatively (model R2 = 0.505, p = 0.010). Conclusion: The lower 1-month postoperative OPN and ucOC levels in PHPT seem to indicate reduced bone resorption. Decreased ucOC levels may also suggest lower energy demands postoperatively.
Ian M Bird, J Ian Mason, William E Rainey
Published: 1 January 1998
Endocrine Research, Volume 24, pp 345-354; https://doi.org/10.3109/07435809809032614

Abstract:
While ACTH receptors (activating the protein kinase A pathway) are expressed throughout the human/bovine/ovine zona glomerulosa (zg) and zona fasciculata (zf), there are clear zonal differences in AII Type-1 receptor levels (activating protein kinase C/Ca2+), as well as resting membrane potential. Thus zg is most responsive to AII and K+ (Ca2+ signalling), while zf is less responsive to AII with no K+ response. Zonal function in turn requires differential expression of CYP17/3betaHSD and CYP11B2/CYP11B1. We have used the H295R cell to study how differential activation of kinase A, kinase C and Ca2+/calmodulin (CaM) kinases may alter the relative expression of the steroidogenic P450s and 3betaHSDII. While CYP11A, CYP17, 3betaHSDII, CYP21, and CYP11B1 are all induced by increases in cAMP, studies with TPA alone or in combination with forskolin reveal subsets of steroidogenic enzymes regulated either positively (CYP21, 3betaHSDII) or negatively (CYP17, CYP11A) by protein kinase C. Thus adrenal 3betaHSDII and CYP21 expression is high in zg and zf, but CYP17 is not expressed in the zg where AII activation of kinase C is highest. In turn both K+ and AII-induced elevation of Ca2+ strongly induces CYP11B2 but not CYP11B1, consistent with preferential expression of CYP11B2 in the zg. We conclude that differential signaling through kinase C and CaM kinases in addition to kinase A underlies zonal differences in both the early and late pathways involved in steroid hormone production within the adrenocortical zones.
Ludwick K. Malendowicz, Paola G. Andreis, , Anna Markowska
Published: 1 January 1996
Endocrine Research, Volume 22, pp 311-318; https://doi.org/10.3109/07435809609030515

Abstract:
The role played by endogenous substance P (SP) in the regulation of hypothalamo-pituitary-adrenal (HPA) axis was investigated in the rat. Normal and ether-stressed (2 min ether-vapor inhalation) or cold-stressed (20 min at 4 degrees C) animals were given a bolus subcutaneous injection of 100 nmol spantide (SPA) a specific antagonist of SP; their blood concentrations of ACTH, aldosterone (ALDO) and corticosterone (B) were measured by specific RIA, 1, 2 or 4 h after the injection. SPA did not evoke significant changes in the basal plasma levels of the three hormones. Ether and cold stresses markedly raised the blood concentrations of ACTH, ALDO and B, being maximal response observed after 1 or 2 h. SPA notably enhanced the responses of the three hormones to ether stress. SPA magnified ALDO and B responses to cold stress, but it notably depressed ACTH one. In light of these findings, it may be concluded that (i) endogenous SP does not affect basal activity of rat HPA axis, but it exerts an inhibitory action on its response to the stresses, especially the ether-inhalation one: and (ii) different mechanisms are involved in the cold and ether stress-induced activation of the HPA axis.
I. M. Bird, J. I. Mason, W. E. Rainey
Published: 1 January 1995
Endocrine Research, Volume 21, pp 169-182; https://doi.org/10.3109/07435809509030432

Abstract:
Human adrenocortical H295R cells express AII receptors which are predominantly of the AT1 but not AT2 subclass. These receptors are functionally coupled to phosphoinositidase C in a manner similar to that seen in fetal human, sheep and bovine adrenocortical cells. Treatment of H295R cells with forskolin or dbcAMP to activate the protein kinase A pathway caused a rapid (maximal by 3 h) and sustained decrease in AT1-R mRNA levels which in turn preceded a time-dependent (maximal by 12 h) and dose-dependent loss of [125I]AII binding and phosphoinositidase C activation on subsequent AII challenge. Thus, both decreased AT1-R mRNA levels and functional receptor expression appear to parallel each other in response to activation of protein kinase A. Activation of the Ca2+/protein kinase C pathways by treatment with AII also caused a rapid (maximal by 3 h) and dose-dependent loss in AT1-R mRNA, but mRNA levels subsequently rose again, approaching control levels by 36 h. Treatment with AII for 48 h had little effect on either [125I]AII binding or the subsequent phosphoinositidase C response. The effect of AII, but not forskolin, was blocked by the presence of cycloheximide. The action of AII on AT1-R mRNA was probably mediated through both protein kinase C and Ca(2+)-sensitive protein kinases as the effect at 4 h was not completely reproduced by phorbol ester alone, but was fully reproduced by a combination of phorbol ester and Ca2+ ionophore. However, increased Ca2+ influx alone, due to treatment with BAYK8644 or elevated extracellular K+, also resulted in a decrease in AT1-R mRNA levels. Thus in the H295R cell, control of AT1-R expression appears to be complex, being achieved at least in part through control of the level of AT1-R mRNA by multiple independent signaling pathways including protein kinase A, protein kinase C and Ca2+.
I. E. Tóth, J. P. Hinson
Published: 1 January 1995
Endocrine Research, Volume 21, pp 39-51; https://doi.org/10.3109/07435809509030419

Abstract:
In this review we defined and classified the neuropeptides (NPs) related to the adrenal gland, according to Palkovits (Frontiers Neuroendocrinol 10:1 1988). The concentration (RIA) and distribution (immunohistochemistry) of NPs, as well as the localization of the receptors (radioligand studies) were summarized. Direct effects of NPs on aldosterone and corticosterone synthesis obtained by in vivo, in situ perfusion, and in vitro experimental approaches were reviewed. Data (from different rat strains and genders) for 35 NPs are presented.
A. R. Gwosdow
Published: 1 January 1995
Endocrine Research, Volume 21, pp 25-37; https://doi.org/10.3109/07435809509030418

Abstract:
The aim of these studies was to determine the intraadrenal mechanism of interleukin-1 (IL-1)-induced corticosterone release from the rat adrenal gland. To accomplish this, the role of catecholamines and eicosanoids on IL-1-induced corticosterone release was determined. Experiments were conducted on primary cultures of dispersed rat adrenal cells. Dose-dependent increases (P < 0.05) in corticosterone concentration were observed when primary adrenal cells were incubated with different doses (10(-10) to 10(-8) M) of IL-1 alpha. IL-1 alpha and IL-1 beta elevated corticosterone release after a 24 hr incubation period. ACTH elevated corticosterone levels at 4 and 24 hr. The stimulatory effect of IL-1 on corticosterone release was mimicked by epinephrine (1 microM), and was selectively blocked by the alpha-adrenergic antagonist, phentolamine (10 microM). The beta-adrenergic antagonist, propranolol (10 microM), did not change IL-1 induced corticosterone release. Neither phentolamine nor propranolol had an effect on ACTH stimulated corticosterone release. Both IL-1 alpha and IL-1 beta significantly elevated (P < 0.05) epinephrine levels after a 24 hr incubation period compared to media-treated controls. Untreated adrenal cells fixed for immunohistochemical staining with a specific anti-rat tyrosine hydroxylase antibody indicate that the primary adrenal cell preparation contained 3.1 +/- 0.45% tyrosine hydroxylase positive cells. On the ultrastructural level, the chromaffin cells were found to be in direct cellular contact with cortical cells. Although IL-1 alpha significantly increased (P < 0.05) prostaglandin E2 (PGE2) levels from primary adrenal cells, the presence of the cyclooxygenase inhibitor, indomethacin (10 microM) significantly inhibited IL-1 alpha-induced PGE2 secretion without altering the effect of IL-1 alpha on corticosterone release. Inhibitors of the lipoxygenase system (5-lipoxygenase, 10 microM) and the lipoxygenase and cytochrome P450 monooxygenase systems (nordihydroguaiaretic acid, 10 microM) did not effect IL-1 alpha-induced corticosterone or PGE2 release. These observations indicate that IL-1 stimulates the local release of catecholamines, which, in turn, stimulates corticosterone release through an alpha-adrenergic receptor; this mechanism is independent of PGE2.
M. Ehrhart-Bornstem, S. R. Bornstein, J. González-Hernández, , M. R. Waterman, W. A. Scherbaum
Published: 1 January 1995
Endocrine Research, Volume 21, pp 13-24; https://doi.org/10.3109/07435809509030417

Abstract:
Sympathoadrenal regulation of adrenocortical steroidogenesis was studied on a physiological, cellular, molecular and morphological level. The effects of nerve activation and of epinephrine (EPI) on adrenal corticosteroid release were compared in isolated perfused pig adrenals with preserved nerve supply. Splanchnic nerve activation as well as perfusion with EPI provoked a significant release of cortisol, aldosterone and androstenedione. In cultured bovine adrenocortical cells steroid secretion and accumulation of P450scc, P450(17) alpha, P450c21 and P450(11) beta mRNAs were studied after stimulation with EPI with or without propranolol or phentolamine. Incubation with EPI stimulated steroidogenesis and increased the levels of all four P450-mRNAs. The beta-adrenergic antagonist propranolol totally blocked the effects of EPI while the alpha-antagonist phentolamine had no effect. Using immunohistochemistry, adrenals were studied morphologically. The contact zones of the two cell types were investigated on an electron microscopical level. Cortical and medullary cells were closely interwoven with cortical and chromaffin cells in direct apposition, providing the possibility for paracrine interactions. It is concluded that the release of corticosteroids can be stimulated through the sympatho-adrenal system. The stimulatory action of EPI upon adrenal steroid formation and accumulation of all four P450-mRNAs requires beta-adrenergic receptors. Taking into consideration the close colocalization of cortical and medullary tissue, this stimulation may be mediated by chromaffin cells in a paracrine manner.
Laura Kragie, Richard Smiehorowski
Published: 1 January 1993
Endocrine Research, Volume 19, pp 207-219; https://doi.org/10.3109/07435809309033025

Abstract:
Hypothyroidism frequently presents with muscle complaints. No consistent histopathology nor electrophysiology explains these symptoms and signs. As well, no previous study shows specific changes in components of the nerve-muscle synapse nor excitation-contraction coupling in adult muscles, but changes are seen in hormone-treated embryonic myoblasts. In this study, adult male Holtzman rats underwent thyroidectomy and their age-matched euthyroid controls were simultaneously subjected to sham operation. Thirty days post-operative, animals were sacrificed for anterior tibialis muscles harvest. Muscle dihydropyridine type calcium channel (isradipine) and acetylcholine receptor (alpha-bungarotoxin) binding were measured and compared between experimental treatment groups. There were no significant differences in either the affinity or density of isradipine binding. However, hypothyroid muscles showed a nearly 50% reduction in acetylcholine receptor density when compared to control muscles. Thyroidectomy is associated with specific effects on components of neuromuscular transmission in adult fast twitch muscle.
Claus Scheidereit, Dietmar Von Der Ahe, , Michael Wenz, , Christopher Carlson, Heinz Bosshard, Hannes M. Westphal,
Published: 1 January 1989
Endocrine Research, Volume 15, pp 417-440; https://doi.org/10.3109/07435808909036347

Abstract:
This work summarizes binding data that were obtained with partially purified glucocorticoid and progesterone receptors, as well as with a crude nuclear protein extract, to DNA sequences in and around hormonally regulated genes. The sequence recognition by the glucocorticoid receptor at the different defined glucocorticoid regulatory elements (GRE) is discussed and a consensus sequence formulated. A three dimensional representation gives an impression of the mode of interaction between the protein and the double helix of DNA. In the promoters of mouse mammary tomour virus (MTV) and chicken lysozyme overlapping binding sites for both, glucocorticoid and progestine-receptors are found that are responsible for the hormonal inducibility of the genes. In crude extract from rat liver nuclei, a nonhistone protein is found that specifically binds to sequences on the MTV-LTR region overlapping the GRE. The possible implication of this protein in hormonal regulation of transcription is discussed.
M. Pettersson, I. Lundquist, B. Ahrén
Published: 1 January 1987
Endocrine Research, Volume 13, pp 407-417; https://doi.org/10.3109/07435808709035466

Abstract:
Neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) are both intrapancreatic neuropeptides that are known to inhibit stimulated insulin secretion. In the present study, we examined their influences on basal and stimulated glucagon and insulin secretion in the mouse. Either NPY or CGRP was injected intravenously at two dose levels (0.85 or 4.25 nmol/kg). When injected alone, neither of them did affect basal plasma glucagon levels but CGRP reduced basal plasma insulin levels. Glucagon secretion stimulated by the cholinergic agonist carbachol was modestly inhibited by NPY at 4.25 nmol/kg (P less than 0.01) but not affected by CGRP. In contrast, glucagon secretion stimulated by the beta 2-adrenoceptor agonist terbutaline was markedly inhibited by NPY already at the lower dose level (P less than 0.01) and potentiated by CGRP (P less than 0.01). Insulin secretion stimulated by carbachol was inhibited by CGRP (P less than 0.01) but not affected by NPY, whereas terbutaline-induced insulin secretion was inhibited by both NPY (P less than 0.05) and CGRP (P less than 0.01). We conclude that the two intrapancreatic neuropeptides NPY and CGRP have opposite actions on stimulated glucagon secretion in the mouse: NPY in an inhibitory and CGRP in a potentiatory direction. Both peptides, however, inhibit insulin secretion stimulated by terbutaline.
J. V. Conaglen, R. A. Donald, E. A. Espiner, J. H. Livesey, M. G. Nicholls
Published: 1 January 1985
Endocrine Research, Volume 11, pp 39-44; https://doi.org/10.3109/07435808509035423

Abstract:
Ovine corticotropin releasing factor (CRF) was administered to six normal men and the plasma ACTH and cortisol responses compared with those following the same dose of CRF (200 micrograms) plus the opiate receptor blocker naloxone (20mg). The addition of naloxone was associated with a significant increase in plasma ACTH, cortisol and aldosterone responses. No change was observed in peripheral plasma levels of epinephrine, norepinephrine, arginine vasopressin, angiotensin II or renin activity in response to CRF plus naloxone. It is concluded that endogenous opioid peptides may inhibit the ACTH response to CRF. However the addition of naloxone does not increase the ACTH response to CRF sufficiently to constitute a useful test of pituitary function.
Susan N. Perkins, Stephen T. Summers, Michael J. Cronin
Published: 1 September 1985
Endocrine Research, Volume 11, pp 181-190; https://doi.org/10.3109/07435808509032976

Abstract:
Beta-adrenergic stimulation of cellular cyclic AMP accumulation was characterized in normal anterior pituitary cells in vitro. In the presence of isobutylmethylxanthine, the order of potency of catecholamine agonists, as well as the antagonism by propranolol and not phentolamine, aided in classifying the receptor as beta-adrenergic. Furthermore, this agonist effect was rapidly desensitized. Tumor promoters, which directly activate protein kinase C, enhanced the cyclic AMP levels achieved with beta-adrenergic agonists (1.5-fold average at 10 min). This acute effect occurred over 10-1000 nM phorbol dibutyrate or phorbol myristate acetate. Finally, 3H-phorbol dibutyrate binding to unstimulated anterior pituitary cells was predominantly associated with the cytosol (79%) versus membrane (21%) fractions. Thus, an acute role for protein kinase C in promoting beta-adrenergic receptor activation of adenylate cyclase activity is suggested for anterior pituitary cells.
Ludwik K. Malendowicz, Piera Rebuffat, Gastone G. Nussdorfer
Published: 1 January 1997
Endocrine Research, Volume 23, pp 131-139; https://doi.org/10.1080/07435809709031848

Abstract:
Substance P (SP) did not affect either basal or agonist-stimulated aldosterone production by dispersed rat zona glomerulosa (ZG) cells. In contrast, the SP-receptor antagonist spantide-II (SPA), at 10−8/10−6 M concentrations, markedly raised basal and 10−9 M ACTH, but not 10−9 M angiotensin II-stimulated aldosterone secretion. The secretagogue effect of 10−6 M SPA was annulled by SP (10−6 M) and the protein kinase (PK)-C inhibitor Ro31-8220 (10−6M), but was unaffected by the PKA inhibitor H-89 (10−5M) In light of these findings the following conclusions can be drawn: (i) SP does not exert a physiologically relevant direct modulatory action on aldosterone secretion of rat ZG cells. (ii) a receptor-independent inhibitory interaction is likely to occur between SP and SPA molecules: and (iii) SPA activates, through a receptor-independent mechanism, phosphoinositide signaling pathway in rat ZG cells.
Ludwick K. Malendowicz, Giuliano Neri, Gastone G. Nussdorfer, Magdalena Nowak, Krystyna Filipiak, Jerry B. Warchol
Published: 1 January 1996
Endocrine Research, Volume 22, pp 175-184; https://doi.org/10.1080/07435809609030506

Abstract:
Substance P (SP) did not change basal corticosterone (B) secretion of dispersed zona fasciculata-reticularis cells of the rat adrenal cortex. Conversely, spantide II (SPA), an antagonist of SP receptors, at a concentration 10(-7)/10(-6) M markedly raised it, and the effect was annulled by equimolar concentrations of SP. Both SP and SPA (10(-6) M) increased cytosolic free calcium concentration in our cell preparations; however, the response to SP was immediate, while that to SPA showed a lag-period of 4-5 min. SP concentration-dependently (from 10(-8) M to 10(-5) M) partially inhibited maximally ACTH (10(-8) M)-induced stimulation of B secretion of dispersed cells, and unexpectedly a similar effect was observed after SPA exposure. In light of these findings, the conclusion is drawn that SP, under basal conditions, does not exert a direct modulatory action of B secretion of rat adrenocortical cells. However, the possibility remains to be explored that SP may play a role in quenching, via a receptor-independent mechanism, the exceedingly high glucocorticoid responses to ACTH of rat adrenocortical cells.
Ludwik K. Malendowicz, Gastone G. Nussdorfer, , Giuseppina Mazzocchi
Published: 1 January 1994
Endocrine Research, Volume 20, pp 307-317; https://doi.org/10.1080/07435809409035866

Abstract:
The effect of a s.c. bolus injection of 2 micrograms galanin on the hypothalamo-pituitary-adrenocortical (HPA) axis were investigated in both normal and ether-stressed (2 min ether-vapor inhalation) or cold-stressed (20 min at 4 degrees C) rats. Blood concentrations of ACTH, aldosterone (ALDO) and corticosterone (B) were measured by specific RIA, 1, 2 or 4 h after galanin injection. Galanin administration to normal rats resulted in a marked rise in the blood levels of ACTH, ALDO and B at 1h and 2 h, the values returned to the baseline after 4 h. Ether and cold stresses notably raised the blood levels of ACTH, ALDO and B, and these rises lasted unchanged until 4 h. Galanin markedly potentiated ACTH and ALDO responses to ether stress at 1 and 2 h, but B response remained unchanged. ACTH response to cold stress was not affected by galanin; however, galanin magnified ALDO response to cold stress at 4 h, and enhanced at 1 h and depressed at 2 h that of B. In light of these findings the following conclusions can be drawn: (i) galanin exerts a stimulatory effect on HPA axis of rats under basal conditions; (ii) under our experimental conditions, ether stress exerts a stronger stimulation of HPA axis than cold stress; (iii) the galaninergic mechanisms involved in the stimulation of ACTH release do not interfere with ether stress-activated ones controlling ACTH secretion, and are probably similar to those underlying the effect of cold stress; (iv) steroidogenic capacity of adrenal cortex, at least in term of glucocorticoid hormones, is a rate-limiting step in the response of rat HPA axis to severe stresses; and (v) galanin exerts a direct secretory action of the rat adrenal gland, that can manifest itself only in the case of submaximally cold stress-stimulated HPA axis.
, , D. Amato, J. Escobedo De La Peña, R. Galván, R. O. Millán‐Guerrero, , A. Zárate, S. Islas‐Andrade
Published: 1 January 2004
Endocrine Research, Volume 30, pp 19-27; https://doi.org/10.1081/erc-120028384

Abstract:
The aim of this survey was to assess the correlation between leptin and insulin sensitivity (IS) in cases of diffuse toxic goiter. This is a descriptive study on patients with diffuse toxic goiter (DTG) assessing their body mass index (BMI), serum leptin concentrations, circulating insulin (area under the curve (AuC) of insulin), average insulin level, thyroid hormones, thyroid stimulating hormone (TSH), glycemia and IS (using a hyperinsulinemic-euglycemic clamp and the homeostasis model for assessment of insulin resistance (HOMA-IR) before and after euthyroidism induced with metimazol. The average patient age was 35 years old (range 31-40 years), height was 157 cm (range 151-160 cm), glycemia was 4.3 +/- 0.3 mmol/L and TSH 0.1 +/- 0.1 microU/mL. Average leptin level was 11.3 +/- 2.8 ng/dL, the average insulin level was 10.13 +/- 3.7 mIU/mL and the AuC for insulin was 50.6 +/- 18 microIU x min/mL. No correlation was found between leptin and BMI, thyroid hormones and glycemia. While controlling for the BMI effect, a correlation was found between leptin and TSH (r = -0.77, p = 0.042), as well as between leptin and insulinemia (r = 0.93, r2 = 0.86, p = 0.001) independently from the state of thyroid function. There was a tendency for a high correlation between leptin and the insulin AuC (hyperthyroidism: r = 0.89, p = 0.056; euthyroidism: r = 0.99, p = 0.056). A negative correlation was found between IS and the insulin AuC (rho = -0.58, p = 0.18). There was a high tendency for correlation between leptin and IS when the BMI effect (HOMA-IR: r = 0.70, p = 0.12; PHE: r = -0.55, p = 0.26) was taken into consideration. There is a high tendency for a negative correlation between leptin and IS when the BMI effect is controlled. There is a high tendency for a positive correlation between leptin and insulin and TSH.
Q. L. Li, P. Feng, T. Satoh, Z. X. Shi, R. Wang, B. D. Weintraub, J. F. Wilber
Published: 1 January 1997
Endocrine Research, Volume 23, pp 297-309; https://doi.org/10.1080/07435809709031859

Abstract:
TRH is negatively regulated by T3 both in the hypothalamic paraventricular nucleus and transient transfection models. Mutations in hTRβ1 genes are associated with the syndrome of generalized resistance to thyroid hormone. To investigate potential effects of mutant TRs on T3 regulation of the hTRH gene, transient gene expression assays were performed in human neuroblastoma (HTB-11) cells with an hTRH promoter-luciferase construct, wild type (WT) hTRβ1, and three qualitatively distinct hTRβ1 mutant forms (ED, OK and PV). In the presence of T3 (10−9 M), liganded WT-hTRβ1 inhibited hTRH promoter activity significantly (40%). Co-transfection of each of the two mutants (ED and OK) achieved similar levels of inhibition only at 10 to 100 fold increased T3 concentrations. Of interest, a 10x excess of mutant ED or OK could also exert dominant negative effects upon WT hTRβ1-T3 mediated inhibitory actions on the hTRH promoter. In contrast, mutant TR-PV exerted neither inhibitory nor dominant negative effects at even higher concentrations of T3. Moreover, all three unliganded mutant forms stimulated TRH promoter activity significantly in the absence of T3, despite their different mutations in the ligand-binding domain (LBD). These data demonstrate that thyroid hormone resistance at the level of TRH gene regulation, due to reduced inhibitory actions of mutant TR-T3 complexes, as well as dominant negative effects upon WT hTRβ1 mediated inhibition, likely contribute to elevated TSH values observed in the syndrome of thyroid hormone resistance.
M. Marazuela, J. A. Vargas, A. Durántez, M. Alvarez-Mon
Published: 1 January 1994
Endocrine Research, Volume 20, pp 291-306; https://doi.org/10.1080/07435809409035865

Abstract:
We examined the proliferative response of T lymphocytes from thirty-eight patients with Graves' disease (17 untreated thyrotoxic and 30 euthyroid on antithyroid medication) to phytohemagglutinin, anti-CD3 MoAb and phorbol esters, as well as the capacities of these lymphocytes to produce interleukin 2 and the density of interleukin 2 receptors and major histocompatibility class II antigens. We found that the response of T lymphocytes to phytohemagglutinin, anti-CD3 monoclonal antibody and phorbol esters from untreated thyrotoxic Graves' disease was significantly enhanced as compared to treated patients and normal controls. Interleukin 2 production by mitogen-triggered T lymphocytes in both treated and untreated patients with Graves' disease was comparable to that of the control population. Interleukin 2 receptor density was found to be normal, whereas that of human leukocyte antigen-DR was increased in both untreated and treated patients. Following lymphocyte stimulation, there was an increase in human leukocyte antigen-DR and interleukin 2 receptor expression in patients with untreated Graves' disease. Significant correlations were found between thyroid hormone concentration and the proliferative responses to the polyclonal mitogen phytohemagglutinin, anti-CD3 monoclonal antibody and phorbol esters in untreated Graves' patients. Furthermore, during the follow-up of 9 patients, attainment of normal thyroid function after antithyroid treatment was associated with a decrease in and normalization of T-proliferative responses. Our data reveal that active Graves' disease is associated with T cell activation and this is probably related to immunological dysregulation as well as to hyperthyroxinemia.
, Sedighe Akrami, Maryam Rahimi, Mohsen Taghizadeh, Masoud Behfar, Mohammad Reza Mazandaranian, Abbas Kheiry, Mohammad Reza Memarzadeh,
Published: 25 July 2017
Endocrine Research, Volume 43, pp 1-10; https://doi.org/10.1080/07435800.2017.1346661

Abstract:
Purpose of the study: There was inconsistent evidence about the benefit of vitamin D plus evening primrose oil (EPO) supplement intake on lipid profiles and reduced oxidative stress among women with polycystic ovary syndrome (PCOS). The current study was performed to evaluate the effects of vitamin D plus EPO supplementation on lipid profiles and biomarkers of oxidative stress in vitamin D-deficient women with PCOS. Materials and methods: This randomized, double-blind, placebo-controlled trial was performed among 60 vitamin D-deficient women with PCOS. Participants were randomly assigned into two groups to receive either 1000 IU vitamin D3 plus 1000 mg EPO (n = 30) or placebo (n = 30) for 12 weeks. Metabolic profiles were quantified at baseline and after the 12-week intervention. Results: Compared with the placebo group, women in vitamin D and EPO co-supplementation group had significant increases in serum 25-hydroxyvitamin D (25(OH)D) (+10.7 ± 8.4 vs. −0.5 ± 1.6 ng/mL, p< 0.001) and plasma total glutathione (GSH) (+62.7 ± 58.0 vs. −0.7 ± 122.7 µmol/L, p = 0.01), while there were significant decreases in triglycerides (−7.3 ± 23.8 vs. +6.9 ± 26.3 mg/dL, p = 0.03), very low-density lipoprotein (VLDL) cholesterol levels (−1.5 ± 4.7 vs. +1.4 ± 5.3 mg/dL, p = 0.03), total/high-density lipoprotein cholesterol ratio (−0.3 ± 0.4 vs. −0.02 ± 0.4, p = 0.02), and malondialdehyde (MDA) concentration (−0.4 ± 0.4 vs. +0.5 ± 1.8 µmol/L, p = 0.008). Conclusion: Overall, vitamin D and EPO co-supplementation for 12 weeks among vitamin D-deficient women with PCOS significantly improved triglycerides, VLDL cholesterol, GSH, and MDA levels.
Xiao Yue Cai, Niranjan Vijayaratnam, Alexander J. B. McEwan, Rebecca Reif,
Published: 25 July 2017
Endocrine Research, Volume 43, pp 11-14; https://doi.org/10.1080/07435800.2017.1346662

Abstract:
Purpose of the study: To compare efficacy of thyroid remnant ablation using 30 mCi or 50 mCi 131-I in papillary thyroid cancer patients. Materials and methods: Five hundred and fifteen consecutive patients with Tumor-Node-Metastasis (TNM) stages T1-T3 N1/N0/NX receiving either 30 mCi or 50 mCi I-131 were analyzed for the effectiveness of remnant ablation using rhTSH-stimulated serum thyroglobulin. One hundred and five consecutive patients receiving 100 mCi I-131 were analyzed for the incidence of radiation thyroiditis and sialadenitis. Results and conclusions: Doses of 30 mCi and 50 mCi were equally effective for low- and moderate-risk disease but 30 mCi was less effective for T1T2NX disease, and 50 mCi was less effective for T3 compared to T1T2 disease. Low dose radiation hypersensitivity or unknown more extensive disease may have accounted for observed differences. Radiation thyroiditis and sialadenitis were more common in a comparison series of 100 mCi dose compared to 30 mCi, but not more common than in 50 mCi doses.
Mary F. Dallman
Published: 1 January 1984
Endocrine Research, Volume 10, pp 213-242; https://doi.org/10.1080/07435808409036499

Abstract:
Adrenocortical growth is discussed with respect to its relation to body weight, elevated ACTH (provoked by sustained stress, adrenal enzyme deficiency, and adrenal enucleation), and unilateral adrenalectomy. It seems likely that these three conditions under which adrenal growth occurs are each controlled and mediated by different agents. Least is known about the growth of adrenals with the growth of the organism; however, because treatment with growth hormone is known to stimulate adrenal mitogenesis, and because adrenals grow in proportion to body growth by increasing cell number, it is proposed that this growth may be mediated by growth hormone (via somatomedin). ACTH causes primarily adrenocortical cellular hypertrophy which is subsequently followed by hyperplasia. It has been shown that the application of a sustained stressor, induction of adrenal enzyme deficiency and adrenal enucleation all result in persistent elevation in circulating ACTH levels and adrenal growth. It appears that the stimulus to ACTH secretion is a virtual or real decrease in corticosteroid feedback signal, and that ACTH secretion is regulated by corticosteroid levels. An additional humoral factor may be triggered by adrenal enucleation, and the possibility that a fragment of the N-terminal peptide of the ACTH precursor molecule plays this role is entertained. Finally, the evidence that the proliferative adrenal growth after unilateral adrenalectomy is mediated by afferent and crossed efferent neural pathways, and is regulated by aldosterone, pineal peptides and exposure to constant light is discussed.
Kelin Chen, Xuehua Jin, , Wei Wang, Yan Wang, Jinchao Zhang
Published: 1 April 2013
Endocrine Research, Volume 38, pp 59-68; https://doi.org/10.3109/07435800.2012.681824

Abstract:
The recent genome-wide association studies reveal that chromosome 3q resides within the linkage region for diabetic nephropathy (DN) in type 1 and type 2 diabetes mellitus (T1D and T2D). The TRPC1 gene is on chromosome 3q22-24, and it has been demonstrated that TRPC1 expression is reduced in the kidney of diabetic animal models. Genetic association of TRPC1 polymorphism with T1D and DN has been reported in European Americans. However, there are no studies reporting the association of TRPC1 genetic polymorphism with T2D with and without DN in Chinese population. This study aimed to demonstrate the genetic role of TRPC1 in the development of T2D with and without DN in Chinese Han population. A genetic association study of TRPC1 was performed in T2D cases and in nondiabetic controls from Han population located in Northern Chinese areas. Six tag single nucleotide polymorphism (SNP) markers derived from HapMap data were genotyped. Among the six SNPs, only rs7638459 was suspected as risk factor of T2D without DN, fitting the log-additive model. The adjusted odds ratio (OR) for the CC genotyping was 2.39 (95% confidence interval (CI) = 1.00-5.68), compared with the TT genotyping. In addition, rs953239 was found to be a protective factor of getting DN in T2D, also fitting the log-additive model. When compared with the AA genotyping for SNP rs953239, the adjusted OR for CC genotyping was 0.63 (95% CI = 0.44-0.99). To summarize, this study shows that TRPC1 genetic polymorphisms are associated with T2D and DN in T2D in the Han Chinese population.
Maya Otto-Duessel, Miaoling He,
Published: 16 May 2012
Endocrine Research, Volume 37, pp 203-215; https://doi.org/10.3109/07435800.2012.668254

Abstract:
Introduction. Androgens regulate a wide array of physiological processes, including male sexual development, bone and muscle growth, and behavior and cognition. Because androgens play a vital role in so many tissues, changes in androgen signaling are associated with a plethora of diseases. How such varied responses are achieved by a single stimulus is not well understood. Androgens act primarily through the androgen receptor (AR), a hormone nuclear receptor that is expressed in a select variety of tissues. Methods. In order to gain a better understanding of how the tissue-selective effects of androgens are achieved, we performed a comparison of microarray data, using previously published datasets and several of our own microarray datasets. These datasets were derived from clinically relevant, AR-expressing tissues dissected from rodents treated with the full androgen dihydrotestosterone (DHT). Results. We found that there is a diverse response to DHT, with very little overlap of androgen regulated genes in each tissue. Gene ontology analyses also indicated that, while several tissues regulate similar biological processes in response to DHT, most androgen regulated processes are specific to one or a few tissues. Thus, it appears that the disparate physiological effects mediated by androgens begin with widely varying effects on gene expression in different androgen-sensitive tissues. Conclusion. The analysis completed in this study will lead to an improved understanding of how androgens mediate diverse, tissue-specific processes and better ways to assess the tissue-selective effects of AR modulators during drug development.
, Yoko Matsuzawa, Hiroko Ito, Masao Omura, Yuzuru Ito, Koichiro Yoshimura, Yuki Yajima, Tomoshige Kino, Tetsuo Nishikawa
Published: 19 October 2010
Endocrine Research, Volume 35, pp 145-154; https://doi.org/10.3109/07435800.2010.497178

Abstract:
Objective. Hyperuricemia, an integral component of metabolic syndrome, is a major health problem causing gout and renal damage. Urine alkalizers such as citrate preparations facilitate renal excretion of the uric acid, but its supportive effect on xanthine oxidase inhibitors has not been tested yet. We performed a randomized, prospective study of the effect of a combination of allopurinol and a citrate preparation on renal function in patients with hyperuricemia, employing 70 patients who had hyperuricemia with serum uric acid levels ≥7.0 mg/dL, or those diagnosed as having hyperuricemia in the past. Methods. They were randomly enrolled into two study groups: the allopurinol monotherapy (MT) group or combination treatment (CT) group with allopurinol and a citrate preparation. Allopurinol (100–200 mg/day) in the absence or presence of a citrate preparation (3 g/day) was administered for 12 weeks and levels of serum uric acid, its urinary clearance (Cua), and the renal glomerular filtration rates assessed with the creatinine clearance (Ccr) were evaluated before and after the treatment. Results. Serum levels of uric acid decreased significantly in both groups, whereas the change observed was much greater in CT group. Cua was significantly increased in CT group but not in MT group. Ccr was not altered in both groups in general, whereas it was significantly increased in a fraction of CT group with decreased renal function. Conclusions. These results indicate that an additional use of citrate preparations with xanthine oxidase inhibitors is beneficial for patients with hyperuricemia, reducing circulating uric acid and improving their glomerular filtration rates.
Published: 1 January 1992
Endocrine Research, Volume 18, pp 91-113; https://doi.org/10.1080/07435809209035401

Abstract:
The present paper summarizes evidence that support the hypothesis of the existence of bilateral interactions between pineal gland and the immune system. Both in vivo and in vitro experiments show that the pineal gland, via its hormone melatonin, enhances immune function. Mechanisms involved in this immunostimulatory effect are not well understood, but some evidence suggests the existence of specific binding sites for melatonin on immune cells. Moreover, the release of opioid peptides and interleukin-2 by T-helper cells may also participate in this mechanism by activating, at least natural killer activity and antibody-dependent cellular cytotoxicity. Some immune signals, i.e., gamma-interferon, may be involved in regulating pineal function, thereby representing a regulatory mechanism in the opposite direction. The physiological and clinical significance of these data remains to be studied.
Karin Zibar Tomšić, Tina Dušek, , Zdravko Heinrich, Mirsala Solak, Ana Vučinović, David Ozretić, Sergej Mihailović Marasanov, Hrvoje Hršak, Darko Kaštelan
Published: 24 May 2017
Endocrine Research, Volume 42, pp 318-324; https://doi.org/10.1080/07435800.2017.1323913

Abstract:
Purpose: The aim of the study was to investigate the incidence of and risk factors for hypopituitarism after gamma knife radiosurgery (GKRS) for pituitary adenoma. Materials and Methods: We conducted a retrospective analysis of the pituitary function of 90 patients who underwent GKRS for pituitary adenoma at the University Hospital Centre Zagreb between 2003 and 2014. Twenty seven of them met the inclusion criteria and the others were excluded from the study due to pituitary insufficiency which was present before GKRS. Eighteen patients had non-functioning and 9 patients had secretory adenomas. Median patients’ age was 56 years (24–82). GKRS was performed using the Leksell gamma knife Model C. The median prescription radiation dose was 20 Gy (15–25) and the median tumor volume size was 3.4 cm3 (0.06–16.81). New onset hypopituitarism was defined as a new deficit of one of the three hormonal axes (corticotroph, thyreotroph, or gonadotroph) ≥3 months following GKRS. SPSS was used for statistical analysis, with the significance level at P<0.05. Results: During the median follow-up period of 72 months (range 6–144), 30% of patients developed new hypopituitarism after GKRS. This corresponds to incidence of one new case of hypopituitarism per 15 patient-years. Age, gender, tumor function, tumor volume, suprasellar extension, prescription dose of radiation, as well as dose-volume to the pituitary gland, stalk and hypothalamus were not predictive factors for the development of hypopituitarism. Conclusions: In our cohort of patients with pituitary tumors who underwent GKRS, 30% developed new hypopituitarism during the follow-up period.
Published: 24 May 2017
Endocrine Research, Volume 42, pp 325-330; https://doi.org/10.1080/07435800.2017.1323914

Abstract:
Background: Mitophagy is a form of autophagy for the elimination of mitochondria. Mitochondrial content and function are reduced in the skeletal muscle of patients with type 2 diabetes mellitus (T2DM). Physical training has been shown to restore mitochondrial capacity in T2DM patients, but the role of mitophagy has not been examined in this context. This study analyzes the impact of a 3-month endurance training on important skeletal muscle mitophagy regulatory proteins and oxidative phosphorylation (OXPHOS) complexes in T2DM patients. Methods: Muscle biopsies were obtained from eight overweight/obese T2DM men (61±10 years) at T1 (6 weeks pre-training), T2 (1 week pre-training), and T3 (3 to 4 days post-training). Protein contents were determined by Western blotting. Results: The training increased mitochondrial complex II significantly (T2–T3: +29%, p = 0.037). The protein contents of mitophagy regulatory proteins (phosphorylated form of forkhead box O3A (pFOXO3A), mitochondrial E3 ubiquitin protein ligase-1 (MUL1), Bcl-2/adenovirus E1B 19-kD interacting protein-3 (BNIP3), microtubule-associated protein 1 light chain-3B (the ratio LC3B-II/LC3B-I was determined)) did not differ significantly between T1, T2, and T3. Conclusions: The results imply that training-induced changes in OXPHOS subunits (significant increase in complex II) are not accompanied by changes in mitophagy regulatory proteins in T2DM men. Future studies should elucidate whether acute exercise might affect mitophagic processes in T2DM patients (and whether a transient regulation of mitophagy regulatory proteins is evident) to fully clarify the role of physical activity and mitophagy for mitochondrial health in this particular patient group.
Siegrid G. A. De Meer, Wessel M. C. M. Vorselaars, Jakob W. Kist, Marcel P. M. Stokkel, , Gerlof D. Valk, Inne H. M. Borel Rinkes,
Published: 16 May 2017
Endocrine Research, Volume 42, pp 302-310; https://doi.org/10.1080/07435800.2017.1319858

Abstract:
Purpose: Differentiated thyroid cancer is the most common endocrine malignancy. Recurrences (5–20%) are the main reason for follow-up. Thyroglobulin (Tg) has proven to be an excellent disease marker, but thyroglobulin-antibodies (Tg-Ab) may interfere with Tg measurement, leading to over or underestimation. It is proposed that the Tg-Ab trend can be used as a marker for disease recurrence, yet few studies define trend and have a long-term follow-up. The objective of our study was to investigate the value of a well-defined Tg-Ab trend as a surrogate marker for disease recurrence during long-term follow-up. Methods: We retrospectively studied patients treated at the Nuclear Department of the University Medical Center Utrecht from 1998 to 2010 and the Netherlands Cancer Institute from 2000 to 2009. All patients with Tg-Ab 12 months after treatment were included. The definition of a rise was >50% increase of the Tg-Ab value in a 2 year time period. A decline as >50% decrease of the Tg-Ab value. Results: Twenty-five patients were included. None of the patients with declining or stable Tg-Ab without a concomitant rise in Tg developed a recurrence. Four patients did suffer a recurrence. Three of these patients had a rising Tg-Ab trend, in two of these patients Tg was undetectable. Conclusions: Tg-Ab trend can be used as a crude surrogate marker for long-term follow-up of Tg-Ab patients. A rising trend in Tg-Ab warrants further investigation to detect recurrent disease. Stable or declining Tg-Ab levels do not seem to reflect a risk for recurrence.
, , , Paraskevas Stamopoulos, Themistoklis Feretis, , , Gerasimos Tsourouflis,
Published: 16 May 2017
Endocrine Research, Volume 42, pp 311-317; https://doi.org/10.1080/07435800.2017.1319859

Abstract:
Carcinogenesis has been related to systematic inflammatory response. Our aim was to study white blood cell and platelet indices as markers of this inflammatory response in thyroid cancer and to associate them with various clinicopathological parameters.
, , , Diego Bailetti, , Flavia A. Cimini, , , , Efisio Cossu, et al.
Published: 7 April 2017
Endocrine Research, Volume 42, pp 331-335; https://doi.org/10.1080/07435800.2017.1305965

Abstract:
Vitamin D acts through the binding to the vitamin D receptor (VDR). Several polymorphisms in VDR gene have been studied. Among these, the rs2228570 C>T (FokI) variant has been demonstrated to be functional, leading to a protein with a different size and activity. So far, genetic studies on the association between VDR gene rs2228570 single nucleotide polymorphism (SNP) and type 2 diabetes mellitus (T2DM) showed contradictory results. Thus, we performed an association study in a large cohort of adult Italian subjects with T2DM and in nondiabetic controls.
Zhao Ya, Liu Fei, Zeng Yue, Liu Dan, Lin Neng-Bo, Luo Yi, Miao Ying,
Published: 23 March 2017
Endocrine Research, Volume 42, pp 296-301; https://doi.org/10.1080/07435800.2017.1300809

Abstract:
Objective: To investigate the association between serum gamma-glutamyl transferase (GGT) levels and serum uric acid levels in middle-aged and elderly Chinese females. Methods: A cross-sectional population survey was performed in Luzhou, China (2014). Questionnaires, physical examinations and biochemical tests were conducted. Finally, we included 2486 females who were > 40 years old as participants. Multiple linear regression analysis was used to estimate the association of serum acid levels and other variables. Serum GGT levels were divided into four groups using the 25th, 50th and 75th percentiles as cut-off points. Finally, binary logistic regression analysis was used to investigate the association of different serum GGT quartiles with the risk of hyperuricemia. Results: The prevalence of hyperuricemia was 25.1% in the studied population and gradually increased across the serum GGT quartiles (P< 0.05). Binary logistic regression analysis showed that compared with subjects in the lowest quartile of serum GGT levels, the adjusted odds ratio (ORs) for uric acid in the highest quartile was 2.34 (95% confidence interval (CI), 1.68–3.28, P< 0.001),after corrections for TG, TC, HDL-C, LDL-C, creatinine (CR), GGT, AST, ALT, fasting plasma glucose (FPG), postprandial 2-h plasma glucose, hemoglobin A1c(HbA1c), age, BMI, SBP, DBP, waist-to-hip ratio and neck circumference (NC). Conclusions: The serum GGT level is associated with hyperuricemia in middle-aged and elderly Chinese females.
, Gustavo García, Bertha Herrero,
Published: 22 March 2017
Endocrine Research, Volume 42, pp 269-280; https://doi.org/10.1080/07435800.2017.1294603

Abstract:
Background: Clinical studies have shown that gestodene (GDN), a potent third-generation synthetic progestin, affects bone resorption. However, its mode of action in bone cells is not fully understood. The aim of this study was to establish whether GDN affects bone directly or through its bioconversion to other metabolites with different biological activities. Methods: In this study, we investigated the effects of GDN and its A-ring reduced metabolites on proliferation, differentiation, and mineralization of calvarial osteoblasts isolated from neonatal rat and their capacity to displace [3H]-E2 at ER binding sites. Results: In contrast to progesterone, gestodene did exert significant effects on osteoblast activities. The most striking finding was the observation that the A-ring reduced derivatives 3β,5α-tetrahydro-GDN and 3α,5α-tetrahydro-GDN, though to a lesser extent, had greater stimulatory effects on the osteoblast activity than those observed with GDN. The effects on osteoblast proliferation and differentiation induced by GDN-reduced derivatives were abolished by the antiestrogen ICI 182780, consistent with their binding affinities for the estrogen receptor. In addition, the presence of a 5α-reductase inhibitor or inhibitors of aldo-keto hydroxysteroid dehydrogenases abolished the GDN-induced enhancement of osteoblast differentiation. These results indicated that GDN is metabolized to the A-ring reduced metabolites with estrogen-like activities and through this mechanism, GDN may affect the osteoblast activity. Conclusion: Together, the data suggest that synthetic progestins derived from 19-nortestosterone such as GDN, have beneficial effects on bone due to their biotransformation into metabolites with intrinsic estrogenic activity.
, Katja Goricar,
Published: 21 March 2017
Endocrine Research, Volume 42, pp 261-268; https://doi.org/10.1080/07435800.2017.1294602

Abstract:
Purpose: Impaired β-cell function remains unaddressed in PCOS. The aim of the study was to evaluate whether dipeptidyl peptidase-4 (DPP-4) inhibitor alogliptin (ALO) alone or in combination with pioglitazone (PIO) improves β-cell function along with insulin resistance (IR) in metformin (MET) treated obese women with PCOS with persistent IR. Materials and methods: In 12-week randomized study, ALO 25 mg QD (n=15) or ALO 25 mg QD and PIO 30 mg QD (n=15) was added to MET 1000 mg BID in PCOS women (aged 34.4 ± 6.5 years, BMI 39.0 ± 4.9 kg/m2, HOMA-IR 4.82 ± 2.52, mean ± SD). Model derived parameters of glucose homeostasis from the meal tolerance test (MTT) were determined. The ability of the β-cell function was assessed by the adaptation index (AI). Results: MET-ALO and MET-ALO-PIO resulted in a significant decrease of HOMA-IR (by 1.6±2.3 (p=0.039) and 2.9±3.3 (p=0.001), respectively) and an increase in insulin sensitivity (IS) after meal ingestion (oral glucose IS) by 31.4±97.5 ml·min–1·m–2 (p=0.007) vs 39.0±58.1 ml·min–1·m–2 (p=0.039), respectively. AI across the entire group was significantly improved from 329.6±200.6 to 442.5±303.9 (p=0.048). Conclusions: ALO alone and in combination with PIO improved IR along with dynamic IS and meal related β-cell function when added to MET treated PCOS.
Hyun-Young Shin, ,
Published: 21 March 2017
Endocrine Research, Volume 42, pp 287-295; https://doi.org/10.1080/07435800.2017.1300808

Abstract:
Purpose: Adiponectin and chemerin have been reported their associations with insulin resistance and chronic inflammation. However, the relationship between adiponectin and chemerin themselves has not been fully elucidated. Therefore, we investigated the effects of changes in adiponectin and chemerin levels after a weight intervention. Materials and methods: We recruited 136 healthy overweight or obese subjects from 2006 to 2009 and provided all participants lifestyle modification therapy with diet consultations over 16 weeks. We assigned the participants to take orlistat or sibutramine or to a no prescription group. We analyzed the data using paired t-tests, Pearson’s partial correlation analysis, and stepwise multiple linear regression analysis. Results: ∆ in chemerin was positively correlated with ∆ in adiponectin (r = 0.29, p< 0.01), and these trends were similar in the insulin-resistant (r = 0.35, p = 0.03) and insulin-sensitive (r = 0.27, p< 0.01) groups. In multiple regression analyses, Δadiponectin, ΔQUICKI (quantitative insulin-sensitivity check index), Δglucose, and ΔDBP were significantly associated with Δchemerin in the insulin-resistant group, and initial chemerin level, ΔQUICKI, ΔBMI (body mass index), and taking orlistat were associated with Δchemerin in the insulin-sensitive group. Conclusions: Changes in chemerin levels were positively associated with changes in adiponectin levels. The association between these changes might be related to chemerin’s dual inflammatory and anti-inflammatory effects or insulin resistance and insulin sensitivity enhancing effects, depending on the metabolic conditions. Additional studies are needed to clarify the mechanisms that underlie the effects of adiponectin and chemerin.
, Tomotada Fujita, Daisuke Suzuki, Tatsuya Nishida, Kazufumi Yamamoto, Ryo Okabayashi, , , Yukihiro Matsuyama
Published: 20 March 2017
Endocrine Research, Volume 15, pp 1-9; https://doi.org/10.1080/07435800.2017.1292527

Abstract:
Monthly regimen of minodronate for osteoporosis more than two years has not been reported yet. The aim of this study is to elucidate the effect of monthly minodronate (M-MIN) on bone mineral density (BMD) and serum pentosidine (Pen) during 27 months.
Haidar Al-Hraishawi, Peter J. Dellatore, , Xiangbing Wang
Published: 20 March 2017
Endocrine Research, Volume 42, pp 1-5; https://doi.org/10.1080/07435800.2017.1292528

Abstract:
Our study supports the hypothesis that iPTH level is associated with TG and HDL levels and should be a factor to consider in the management of PHPT patients.
, González-Sánchez Ignacio, Marco A. Cerbón Cervantes
Published: 20 March 2017
Endocrine Research, Volume 76, pp 1-13; https://doi.org/10.1080/07435800.2017.1292526

Abstract:
Purpose: This study was designed to investigate whether estradiol is related to the expression of the chemokine receptor CXCR4 and its activation in lung adenocarcinoma in vitro, since lung adenocarcinomas from premenopausal women have shown high levels of CXCR4, and this expression has been associated with worse prognosis and poor survival. Methods: The effect of 17-β-estradiol (E2) (0.03 nM-10 nM) on CXCR4 expression was analyzed in lung adenocarcinoma cell lines (SK-LU-1, H1435, H23, A549) by immunofluorescence after 24 and 72-h poststimulation. Tamoxifen treatment was applied to corroborate the estrogenic effect. The wound-healing assay was performed to investigate whether E2 treatment increased CXCR4/CXL12 pathway activity. A549 and SK-LU-1 cells were stimulated with E2, CXCL12, and CXCL12 combined with E2. Tamoxifen and AMD3100 were applied to corroborate estrogen and chemokine pathway activation. Results: Estradiol stimulated significantly CXCR4 overexpression in all the cell lines analyzed in a dose- and a time-dependent manner. Tamoxifen treatment inhibited the CXCR4 overexpression observed in estrogen-treated groups, demonstrating that estrogen strongly influences CXCR4 expression in lung adenocarcinoma cells. Cells treated with E2, CXCL12 and E2 combined with CXCL12 exhibited significant cell migration, which was suppressed when tamoxifen and AMD3100 were present. Conclusion: Overexpression of CXCR4 induced by estrogen and the activity of CXCL12/CXCR4 pathway could be a new mechanism by which this hormone supports tumor progression and metastasis. These findings may partly explain the worse prognosis observed in premenopausal women and suggest considering the role of estrogen in lung cancer for the design of more specific treatment schemes.
Maria Del Carmen Ortiz Segura, Blanca Estela Del Río Navarro, Benjamín Antonio Rodríguez Espino, , , Santiago Villafaña, Enrique Hong, Fabián Meza-Cuenca, Patrick Mailloux Salinas, Francisco Javier Bolanos Jimenez, et al.
Published: 20 March 2017
Endocrine Research, Volume 42, pp 1-8; https://doi.org/10.1080/07435800.2017.1294601

Abstract:
Purpose: The aim of this study was to investigate the possible relationship among insulin resistance (IR), endothelial dysfunction, and alteration of adipokines in Mexican obese adolescents and their association with metabolic syndrome (MetS). Materials and methods: Two hundred and twenty-seven adolescents were classified according to the body mass index (BMI) (control: N=104; obese: N=123) and homeostasis model of the assessment-insulin resistance index (HOMA-IR) (obese with IR: N=65). The circulating concentrations of leptin, adiponectin, soluble intercellular adhesion molecule-1 (sICAM-1), and IR were determined by standard methods. Results: The obese adolescents with IR presented increased presence of MetS and higher circulating concentrations in sICAM-1 in comparison with the obese subjects without IR. The lowest concentrations of adiponectin were observed in the obese with IR. In multivariate linear regression models, sICAM-1 along with triglycerides, total cholesterol, and waist circumference was strongly associated with HOMA-IR (R2=0.457, P=0.008). Similarly, after adjustment for age, BMI-SDS, lipids, and adipokines, HOMA-IR remained associated with sICAM-1 (R2=0.372, P=0.008). BMI-SDS was mildly associated with leptin (R2=0.176, P=0.002) and the waist circumference was mild and independent determinant of adiponectin (R2=0.136, P=0.007). Conclusions: Our findings demonstrated that the obese adolescents, particularly the obese subjects with IR exhibited increased presence of MetS, abnormality of adipokines, and endothelial dysfunction. The significant interaction between IR and endothelial dysfunction may suggest a novel therapeutic approach to prevent or delay systemic IR and the genesis of cardiovascular diseases in obese patients.
He Wenjing, Yu Shuang, Li Weisong, Xiao Haipeng
Published: 20 March 2017
Endocrine Research, Volume 86, pp 1-10; https://doi.org/10.1080/07435800.2017.1292525

Abstract:
Glucagon-like peptide-1 (GLP-1) receptor agonists are a kind of very popular antidiabetes drugs. They promote cell proliferation and survival through activation of signaling pathways in human islet cells involving phosphate idylinositol 3 kinase (PI3K) and extracellular regulated kinases 1 and 2 (ERK1/2), which are frequently activated in human colon cancer cells. Then, it is possible that taking GLP-1 receptor (GLP-1R) agonists persistently would induce proliferation of β cells as well as colon cancer cells. So, clarifying the effects and mechanisms of GLP-1R agonists on colon cancer cells has important clinical implications.
Nadide Melike Sav, , Leyla Akin,
Published: 20 March 2017
Endocrine Research, Volume 42, pp 281-286; https://doi.org/10.1080/07435800.2017.1295982

Abstract:
The urinary excretions of Pyr and DPyr are higher in diabetic subjects than in healthy controls, suggesting the presence of increased bone turnover in diabetic patients, but we could not observe any negative effect of childhood diabetes on BMD. These results may suggest that diabetic patients are at risk for a decreased peak bone mass.
, Kursat Dal, , Murat Eser, Fatma Kaplan Efe, , Kubilay Şahin, Salih Baser, Naim Ata, Aysun Aybal Kutlugun, et al.
Published: 13 March 2017
Endocrine Research, Volume 42, pp 1-6; https://doi.org/10.1080/07435800.2017.1293686

Abstract:
In this study, we evaluated creatinine and eGFR levels in patients with hypothyroidism and found out that renal function improved in most patients after euthyroidism was achieved. In some patients, above-normal creatinine levels completely returned to normal once the patients became euthyroid.
Hossein Darabi, , , Mohammadreza Kalantarhormozi, , Samad Akbarzadeh, , , ,
Published: 13 March 2017
Endocrine Research, Volume 97, pp 1-7; https://doi.org/10.1080/07435800.2017.1292523

Abstract:
The adipocytokines and insulin-like growth factor 1 (IGF-1) are involved in insulin resistance, the cardiometabolic syndrome, and atherosclerosis. Therefore, investigating the relationship between circulating levels of the novel adipocytokines and IGF-1 is worthwhile. The correlation between IGF-1, visfatin, and omentin-1 has not been adequately investigated. In a population-based study, 324 postmenopausal women were randomly selected. Circulating IGF-1, visfatin, omentin-1, adiponectin, and high-sensitivity C-reactive protein (hs-CRP) levels were measured with the highly specific enzyme-linked immunosorbent assay method. In multiple regression analyses adjusted for alkaline phosphatase, osteocalcin, and hs-CRP, circulating IGF-1 was significantly correlated with visfatin levels (standardized β coefficient [β] = 0.13, partial correlation coefficient [r] = 0.12, p = 0.028). The significant positive correlation between serum IGF-1 and visfatin levels remained after additional adjustments for age and BMI (β = 0.12, r = 0.12, p = 0.025), metabolic syndrome (β = 0.13, r = 0.12, p = 0.021), and type 2 diabetes mellitus (β = 0.13, r = 0.12, p = 0.026). No significant correlations were found between IGF-1, adiponectin, and omentin-1. There is a significant correlation between serum IGF-1 and visfatin levels in postmenopausal women beyond metabolic syndrome, type 2 diabetes, bone formation markers, and hs-CRP levels. The observed correlation between higher circulating IGF-1 and the higher visfatin levels might be a physiological compensation and adaptation to protect against visfatin-induced proinflammatory effects.
Yuthika Malhotra, Rajeev Mohan Kaushik,
Published: 13 March 2017
Endocrine Research, Volume 10, pp 1-11; https://doi.org/10.1080/07435800.2017.1292524

Abstract:
Purpose: To study the prevalence of left ventricular diastolic dysfunction (LVDD) in patients with subclinical hypothyroidism (SCH) and the response of LVDD to L-thyroxine therapy. Materials and methods: This cross-sectional case–control study with one longitudinal arm included 67 patients with SCH attending a tertiary care hospital in Uttarakhand, India, and 67 age- and sex-matched healthy controls. LVDD was assessed by 2D, pulsed-wave Doppler (PWD), continuous wave Doppler (CWD), and tissue Doppler echocardiography (TDE). Patients with LVDD received L-thyroxine therapy with reassessment for LVDD 6 months later. Results: SCH patients had a higher prevalence of LVDD than controls (13.43% versus 1.49%; p = 0.017). LVDD showed a significant association with gender (p = 0.004) and serum FT4 (p = 0.001). E velocity, E’ velocity, A’ velocity, iso-volumetric relaxation time (IVRT), E/A, and E’/A’ ratios were significantly lower, while A velocity, deceleration time (DT), E/E’ ratio, left atrial (LA) volume index, and peak tricuspid regurgitation (TR) velocity were significantly higher in cases than controls (p< 0.05 each). The E/A ratio correlated significantly with age, serum very low-density lipoprotein (VLDL), triglycerides (TG), thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and high-density lipoprotein (HDL) (p< 0.05 each). E’ velocity correlated significantly with age, serum total cholesterol, VLDL, and TG (p< 0.05 each), DT with serum total cholesterol (p = 0.047), and LA volume index with age (p = 0.021). Age (p = 0.016) and serum HDL (p = 0.029) were independent predictors of E/A ratio. Gender was an independent predictor for LVDD (p = 0.003). Echocardiographic indices for LVDD showed significant improvement after 6 months of L-thyroxine therapy (p< 0.05 each). Conclusions: LVDD occurs commonly in SCH patients. It can be detected timely using echocardiography and may be reversed by L-thyroxine therapy.
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