Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 14, Issue -, Pages 2983-2995Publisher
BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/3428
Keywords
SIRT1; NAMPT; NAD Biosynthesis; Insulin Secretion; Insulin Sensitivity; Type 2 Diabetes; Pancreatic Beta Cells; Liver; Skeletal Muscle; Adipose Tissue; PBEF; visfatin; Review
Categories
Funding
- National Institute on Aging [AG024150]
- Ellison Medical Foundation
- American Diabetes Association
- Juvenile Diabetes Research Foundation
- Glenn Award for Research in Biological Mechanisms of Aging
- Washington University Clinical Nutrition Research Unit [DK56341]
- National Center for Research Resources [C06RR015502]
- German Research Council [KFO 152]
- NATIONAL CENTER FOR RESEARCH RESOURCES [C06RR015502] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK056341] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG024150] Funding Source: NIH RePORTER
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Both genetic and environmental factors contribute to the pathogenesis of type 2 diabetes, and it is critical to understand the interplay between these factors in the regulation of insulin secretion and insulin sensitivity to develop effective therapeutic interventions for type 2 diabetes. For the past several years, studies on the mammalian NAD-dependent protein deacetylase SIRT1 and systemic NAD biosynthesis mediated by nicotinamide phosphoribosyltransferase (NAMPT) have demonstrated that these two regulatory components together play a critical role in the regulation of glucose homeostasis, particularly in the regulation of glucose-stimulated insulin secretion in pancreatic beta cells. These components also contribute to the age-associated decline in beta cell function, which has been suggested to be one of the major contributing factors to the pathogenesis of type 2 diabetes. In this review article, the roles of SIRT1 and NAMPT-mediated systemic NAD biosynthesis in glucose homeostasis and the pathophysiology of type 2 diabetes will be summarized, and their potential as effective targets for the treatment and prevention of type 2 diabetes will be discussed.
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