An overview of pancreatic beta-cell defects in human type 2 diabetes: implications for treatment

Regul Pept. 2008 Feb 7;146(1-3):4-11. doi: 10.1016/j.regpep.2007.08.017. Epub 2007 Aug 29.


Type 2 diabetes is the most common form of diabetes in humans. It results from a combination of factors that impair beta-cell function and tissue insulin sensitivity. However, growing evidence is showing that the beta-cell is central to the development and progression of this form of diabetes. Reduced islet and/or insulin-containing cell mass or volume in Type 2 diabetes has been reported by several authors. Furthermore, studies with isolated Type 2 diabetic islets have consistently shown both quantitative and qualitative defects of glucose-stimulated insulin secretion. The impact of genotype in affecting beta-cell function and survival is a very fast growing field or research, and several gene polymorphisms have been associated with this form of diabetes. Among acquired factors, glucotoxicity, lipotoxicity and altered IAPP processing are likely to play an important role. Interestingly, however, pharmacological intervention can improve several defects of Type 2 diabetes islet cells in vitro, suggesting that progression of the disease might not be relentless.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cell Count
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / etiology*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Fatty Acids, Nonesterified / pharmacology
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / pathology*
  • Metformin / therapeutic use*


  • Fatty Acids, Nonesterified
  • Hypoglycemic Agents
  • Insulin
  • Metformin