Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis
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TLDR
In type 1 and type 2 diabetes impairment of beta cell function is an early feature of disease pathogenesis while a substantial decrease in beta cell mass occurs more closely to clinical manifestation, which suggests that the development of novel strategies for protection and recovery ofBeta cell function could be most promising for successful diabetes treatment and prevention.Abstract:
Background
Plasma insulin levels are predominantly the product of the morphological mass of insulin producing beta cells in the pancreatic islets of Langerhans and the functional status of each of these beta cells. Thus, deficiency in either beta cell mass or function, or both, can lead to insufficient levels of insulin, resulting in hyperglycemia and diabetes. Nonetheless, the precise contribution of beta cell mass and function to the pathogenesis of diabetes as well as the underlying mechanisms are still unclear. In the past, this was largely due to the restricted number of technologies suitable for studying the scarcely accessible human beta cells. However, in recent years, a number of new platforms have been established to expand the available techniques and to facilitate deeper insight into the role of human beta cell mass and function as cause for diabetes and as potential treatment targets.read more
Citations
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Circadian Etiology of Type 2 Diabetes Mellitus
TL;DR: The aim of this review will be to outline the rationale for therapeutic targeting of the circadian system in the treatment and prevention of Type 2 diabetes mellitus and consequent metabolic comorbidities.
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Dysfunction of Persisting β Cells Is a Key Feature of Early Type 2 Diabetes Pathogenesis.
Christian M. Cohrs,Julia K. Panzer,Denise M. Drotar,Stephen J. Enos,Nicole Kipke,Chunguang Chen,Robert Bozsak,Eyke Schöniger,Florian Ehehalt,Marius Distler,Ana Brennand,Stefan R. Bornstein,Jürgen Weitz,Michele Solimena,Stephan Speier +14 more
TL;DR: It is shown that, in tissue of pre-diabetic, impaired glucose-tolerant subjects, β cell volume is unchanged, but function significantly deteriorates, exhibiting increased basal release and loss of first-phase insulin secretion, and in individuals with type 2 diabetes, function within the sustainedβ cell volume further declines.
Journal ArticleDOI
Nutrient Metabolism, Subcellular Redox State, and Oxidative Stress in Pancreatic Islets and β-Cells
TL;DR: The data indicated that the nutrient regulation of β-cell redox signaling and ROS toxicity is far more complex than previously thought, and that the subcellular compartmentation of these processes cannot be neglected when evaluating the mechanisms of ROS production or the efficacy of antioxidant enzymes and antioxidant drugs under glucolipotoxic conditions and in T2D.
Journal ArticleDOI
Beta-Cell Mass in Obesity and Type 2 Diabetes, and Its Relation to Pancreas Fat: A Mini-Review.
Jun Inaishi,Yoshifumi Saisho +1 more
TL;DR: The current knowledge on beta-cell mass, beta- cell function, and pancreas fat in obesity and T2DM is summarized, and treatment strategies for T2 DM are discussed in relation to Beta-cell preservation.
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Type 2 diabetes
TL;DR: In this paper , a clinically focused review of the recent developments in type 2 diabetes care including controversies and future directions is presented. But despite advances, substantial barriers to changing the course of the epidemic remain.
References
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Genome-Wide Association Analysis Identifies Loci for Type 2 Diabetes and Triglyceride Levels
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A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants.
Laura J. Scott,Karen L. Mohlke,Lori L. Bonnycastle,Cristen J. Willer,Yun Li,William L. Duren,Michael R. Erdos,Heather M. Stringham,Peter S. Chines,Anne U. Jackson,Ludmila Prokunina-Olsson,Chia-Jen Ding,Amy J. Swift,Narisu Narisu,Tianle Hu,Randall Pruim,Rui Xiao,Xiao-Yi Li,Karen N. Conneely,Nancy Riebow,Andrew G. Sprau,Maurine Tong,Peggy P. White,Kurt N. Hetrick,Michael W. Barnhart,Craig W. Bark,Janet L. Goldstein,Lee Watkins,Fang Xiang,Jouko Saramies,Thomas A. Buchanan,Richard M. Watanabe,Timo T. Valle,Leena Kinnunen,Gonçalo R. Abecasis,Elizabeth W. Pugh,Kimberly F. Doheny,Richard N. Bergman,Jaakko Tuomilehto,Francis S. Collins,Michael Boehnke +40 more
TL;DR: The number of T2D loci now confidently identified to at least 10 is confirmed, and it is confirmed that variants near TCF7L2, SLC30A8, HHEX, FTO, PPARG, and KCNJ11 are associated with T1D risk.