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ISSN / EISSN : 00121797 / 1939327X
Current Publisher: American Diabetes Association (10.2337)
Total articles ≅ 31,504
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Latest articles in this journal

Mona S. Nilsen, Regine Å. Jersin, Arve Ulvik, André Madsen, Adrian McCann, Per-Arne Svensson, Maria E. Svensson, Bjørn G. Nedrebø, Oddrun A. Gudbrandsen, Grethe S. Tell, et al.
Published: 25 June 2020
Diabetes; doi:10.2337/db19-1174

Jessie M. Barra, Veronika Kozlovskaya, Eugenia Kharlampieva, Hubert M. Tse
Published: 25 June 2020
Diabetes; doi:10.2337/db20-0248

Published: 19 June 2020
Diabetes, Volume 69, pp 1309-1310; doi:10.2337/db20-ti07

Abstract:
By Max Bingham, PhD T cells that are reactive to hybrid insulin peptides (HIPs) can be detected at much higher rates in peripheral blood of individuals with type 1 diabetes, according to Arribas-Layton et al. ( p. 1492 ). Specifically, they report a new class of HIPs associated with the HLA-DRB1*04:01 allele, which is part of the high-risk type 1 diabetes–associated DR4/DQ8 haplotype, and that they may activate pathogenic CD4+ T cells, potentially explaining loss of insulin secretion from pancreatic β-cells. Their approach involved bioinformatics screening of a library of theoretical HIP sequences derived from insulin or other islet-derived protein fragments to identify potential peptides for further screening in vitro. After additional confirmatory steps, the authors then selected six HIPs to take further in the investigation. They found that T cells that recognize these HIPs are present in the peripheral blood of some individuals with type 1 diabetes, although there was considerable diversity present. For example, some had high frequencies of T cells for multiple HIPs, whereas others had very few HIP-reactive T cells. Age was reportedly the only characteristic that significantly correlated with the combined frequency of HIP-reactive cells. Further investigations showed that the CD4+ T cells that recognize the HIPs also exhibited an effector memory phenotype and reacted to islet preparations. The authors also investigated the presence of HIP-reactive T cells in control subjects, and while they did detect the presence of some HIP-reactive CD4+ T cells, these were present at significantly lower levels than in individuals with type 1 diabetes. Commenting more widely, author Eddie A. James told Diabetes : “Discovery of this new class of HIP-reactive T cells is an important confirmation that nongenetically encoded peptides play a role in breaking tolerance. …
Joana Almaça, Alejandro Caicedo
Published: 19 June 2020
Diabetes, Volume 69, pp 1336-1338; doi:10.2337/dbi20-0016

Abstract:
The pancreatic islet is a highly vascularized endocrine mini-organ that depends on blood supply to function efficiently. As blood flows through islet capillaries reaching different endocrine cell types, it significantly impacts nutrient sensing, paracrine communication, and the final hormonal output. Thus, any change in blood flow, either induced physiologically (e.g., nervous input) or as a result of pathological changes (e.g., fibrosis), could affect islet function. It is not a stretch to state that the way the islet vasculature is arranged anatomically and regulated functionally must have consequences for glucose homeostasis. Despite its potential impact for islet function, interest in the islet vasculature has been sporadic and is certainly not equal to that professed to the cells it serves. Still, there has been a substantive research effort in this arena. From beautiful scanning electron images of corrosion casts (1) to creative physiological experiments using perfused pancreases (2) and microbeads (3), investigators have employed various approaches to study the microcirculation of the islet. The results of these studies provided structural and functional insight but also raised questions. To settle a debate that had started in the mid-1960s, a group of prominent islet biologists decided to meet in 1996 to review existing notions about islet blood flow and “agreed to disagree” that there were three models (4). In model 1, non–β-cells are perfused before β-cells, allowing other endocrine cells to influence β-cells located downstream. In model 2, β-cells are perfused before the other endocrine cells and thus dominate islet function. In model 3, there is no apparent order of perfusion, but blood …
John M. Lachin, David M. Nathan, Bernard Zinman, Ionut Bebu
Published: 19 June 2020
Diabetes, Volume 69; doi:10.2337/db20-0311

Abstract:
In “Understanding Metabolic Memory: A Tale of Two Studies,” Miller and Orchard (1) purportedly disprove “metabolic memory.” However, their analyses do not directly address metabolic memory and their interpretations are flawed. The Diabetes Control and Complications Trial (DCCT) (2) demonstrated that randomly assigned intensive therapy, with mean HbA1c of ∼7%, dramatically reduced microvascular complications compared with conventional therapy, with mean HbA1c of ∼9%, an effect entirely attributable to the separation in HbA1c levels between the two groups (3). Afterward, all participants were taught intensive therapy and referred to their physicians for care, resulting in similar HbA1c levels of ∼8% in the two original groups. This would have been predicted to narrow the rate of complications between the original groups. However, with …
Rachel G. Miller, Trevor J. Orchard
Published: 19 June 2020
Diabetes, Volume 69; doi:10.2337/dbi20-0021

Abstract:
We agree with Lachin et al. (1) that intensive therapy should be started as early as possible after type 1 diabetes onset. The concept of cumulative glycemic exposure in no way alters that clinical message. The intention of our article (2) was to raise the argument that “metabolic memory” has been accepted without a full exploration of a simpler alternative explanation for the observed persistence of benefit in the intensive therapy arm after Diabetes Control and Complications Trial (DCCT) closeout. Importantly, we do not “purportedly disprove metabolic memory” (1) but merely suggest “There is no need [our emphasis] to invoke a ‘metabolic memory’ phenomenon to explain the persistence of a lower incidence of complications …
Eddie A. James, Roberto Mallone, Sally C. Kent, Teresa P. DiLorenzo
Published: 19 June 2020
Diabetes, Volume 69, pp 1311-1335; doi:10.2337/dbi19-0022

The publisher has not yet granted permission to display this abstract.
Published: 19 June 2020
Diabetes, Volume 69, pp 1597-1597; doi:10.2337/db20-ie07

Abstract:
The American Diabetes Association is dedicated to ensuring that you stay informed of the latest COVID-19 research and guidelines. Our new online page for diabetes professionals includes essential resources and information—including webinars, patient guidance, relevant news articles, a discussion forum, and more. Follow updates and join the conversation at professional.diabetes.org/content-page/covid-19. In this special podcast series, Drs. Neil Skolnik and John J. Russell of Abington …
Ingrid Lovise Augestad, Hiranya Pintana, Martin Larsson, Camilla Krizhanovskii, Thomas Nyström, Thomas Klein, Vladimer Darsalia, Cesare Patrone
Published: 15 June 2020
Diabetes; doi:10.2337/db20-0095

The publisher has not yet granted permission to display this abstract.
Kung-Hsien Ho, Xiaodun Yang, Anna B. Osipovich, Over Cabrera, Mansuo L. Hayashi, Mark A. Magnuson, Guoqiang Gu, Irina Kaverina
Published: 15 June 2020
Diabetes; doi:10.2337/db19-1186

The publisher has not yet granted permission to display this abstract.
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