Pancreatic β-cell proliferation in obesity

Adv Nutr. 2014 May 14;5(3):278-88. doi: 10.3945/an.113.005488. Print 2014 May.


Because obesity rates have increased dramatically over the past 3 decades, type 2 diabetes has become increasingly prevalent as well. Type 2 diabetes is associated with decreased pancreatic β-cell mass and function, resulting in inadequate insulin production. Conversely, in nondiabetic obesity, an expansion in β-cell mass occurs to provide sufficient insulin and to prevent hyperglycemia. This expansion is at least in part due to β-cell proliferation. This review focuses on the mechanisms regulating obesity-induced β-cell proliferation in humans and mice. Many factors have potential roles in the regulation of obesity-driven β-cell proliferation, including nutrients, insulin, incretins, hepatocyte growth factor, and recently identified liver-derived secreted factors. Much is still unknown about the regulation of β-cell replication, especially in humans. The extracellular signals that activate proliferative pathways in obesity, the relative importance of each of these pathways, and the extent of cross-talk between these pathways are important areas of future study.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Proliferation*
  • Diabetes Mellitus, Type 2 / metabolism
  • Diet, High-Fat / adverse effects
  • Disease Models, Animal
  • Hepatocytes / metabolism
  • Humans
  • Hyperglycemia / metabolism
  • Insulin Resistance
  • Insulin-Secreting Cells / cytology*
  • Liver / metabolism
  • Obesity / metabolism*
  • Receptors, G-Protein-Coupled / metabolism


  • Receptors, G-Protein-Coupled