Abstract
Type 2 diabetes is characterized by decreased functional beta-cell mass, as a consequence of metabolic stress associated with obesity, aging, insulin resistance and pregnancy. The metabolic stress is caused by increased insulin demand, pro-inflammatory cytokines, and free fatty acids. Fortunately, islets have remarkable property to adapt to increased metabolic demand. This review focuses on the mechanisms of islet adaptation to metabolic stress in obesity and insulin resistance
Keywords: Islets, adaptation, hypertrophy, epigenetics, beta-cells, models.
Current Diabetes Reviews
Title:Islet Compensation in Metabolic Stress: Lessons from Animal Models
Volume: 12 Issue: 4
Author(s): Himadri Singh
Affiliation:
Keywords: Islets, adaptation, hypertrophy, epigenetics, beta-cells, models.
Abstract: Type 2 diabetes is characterized by decreased functional beta-cell mass, as a consequence of metabolic stress associated with obesity, aging, insulin resistance and pregnancy. The metabolic stress is caused by increased insulin demand, pro-inflammatory cytokines, and free fatty acids. Fortunately, islets have remarkable property to adapt to increased metabolic demand. This review focuses on the mechanisms of islet adaptation to metabolic stress in obesity and insulin resistance
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Cite this article as:
Singh Himadri, Islet Compensation in Metabolic Stress: Lessons from Animal Models, Current Diabetes Reviews 2016; 12 (4) . https://dx.doi.org/10.2174/1573399811666150617161915
DOI https://dx.doi.org/10.2174/1573399811666150617161915 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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