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 NAMPTmediated 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.

Original languageEnglish
Pages (from-to)2983-2995
Number of pages13
JournalFrontiers in Bioscience
Issue number8
StatePublished - Jan 1 2009


  • Adipose tissue
  • Insulin secretion
  • Insulin sensitivity
  • Liver
  • NAD biosynthesis
  • PBEF
  • Pancreatic beta cells
  • Review
  • SIRT1
  • Skeletal muscle
  • Type 2 diabetes
  • Visfatin


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