Increased circadian prolactin release is blunted after body weight loss in obese premenopausal women
- 1 February 2006
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Endocrinology and Metabolism
- Vol. 290 (2), E218-E224
- https://doi.org/10.1152/ajpendo.00156.2005
Abstract
We recently showed that prolactin (PRL) release is considerably enhanced in obese women in proportion to the size of their visceral fat mass. PRL release is inhibited by dopamine 2 receptor (D2R) activation, and dietary restriction/weight loss are associated with increased dopaminergic signaling in animals. Therefore, we hypothesized that enhanced PRL release in obese humans would be reversed by weight loss. To evaluate this postulate, we measured 24-h plasma PRL concentrations at 10-min intervals in 11 obese premenopausal women (BMI 33.3 ± 0.7 kg/m2) before and after weight loss (50% reduction of overweight/15% absolute weight loss, using a very low-calorie diet) in the follicular phase of their menstrual cycle. The 24-h PRL concentration profiles were analyzed by a peak detection program (Cluster) and a wave form-independent deconvolution technique (Pulse). Spontaneous 24-h PRL secretion was significantly reduced in obese women [mean daily release, before 128 ± 24 vs. after weight loss 110 ± 17 μg/liter distribution volume (Vdl)−1 × 24 h, P = 0.05]. Body weight loss particularly blunted PRL secretory burst mass (Pulse area, before 230 ± 28 vs. after weight loss 221 ± 31 μg/Vdl−1 × 24 h, P = 0.03), whereas burst frequency was unaffected (no. of pulses, before 11 ± 1 vs. after weight loss 12 ± 1 n/24 h, P = 0.69). Thus elevated PRL secretion rate in obese women is significantly reduced after loss of 50% of overweight. We speculate that amelioration of deficit D2R-mediated neurotransmission and/or diminutions of circulating leptin/estrogen levels might be involved in the physiology of this phenomenon.Keywords
This publication has 38 references indexed in Scilit:
- Functional studies of the kidney of living animals using multicolor two-photon microscopyAmerican Journal of Physiology-Cell Physiology, 2002
- Dopamine as a Prolactin (PRL) InhibitorEndocrine Reviews, 2001
- Body Weight and Fat Deposition in Prolactin Receptor-Deficient Mice**This work was supported in part by grants from the NICHD (HD-24192 to M.F.), the Juvenile Diabetes Foundation (196029 to M.F.), Eli Lilly & Co. (to M.F.), and INSERM (to P.A.K.).Endocrinology, 2001
- Prolactin (PRL) and Its Receptor: Actions, Signal Transduction Pathways and Phenotypes Observed in PRL Receptor Knockout MiceEndocrine Reviews, 1998
- The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDMDiabetes, 1988
- Robust Locally Weighted Regression and Smoothing ScatterplotsJournal of the American Statistical Association, 1979
- SIMULTANEOUS STUDY OF CORTISOL, GROWTH HORMONE AND PROLACTIN NYCTOHEMERAL VARIATIONS IN NORMAL AND OBESE SUBJECTS. INFLUENCE OF PROLONGED FASTING IN OBESITYClinical Endocrinology, 1978
- Alterations in Basal and TRH-Stimulated Serum Levels of Thyrotropin, Prolactin, and Thyroid Hormones in Starved Obese MenJournal of Clinical Endocrinology & Metabolism, 1977
- Estrogen Potentiation of Phenothiazine-Induced Prolactin Secretion in ManJournal of Clinical Endocrinology & Metabolism, 1973
- Catecholamine synthesis and the regulation of food intake in the ratLife Sciences, 1973