The stress of starvation: glucocorticoid restraint of beta cell development

Diabetologia. 2011 Feb;54(2):223-6. doi: 10.1007/s00125-010-1963-x. Epub 2010 Nov 12.


Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this effect of under-nutrition on beta cell mass and that even at physiological levels they restrain fetal beta cell development in utero. There are emerging clues that this occurs downstream of endocrine commitment by neurogenin 3 but prior to terminal beta cell differentiation. Deciphering the precise mechanism will be important as it might unveil new pathways by which to manipulate beta cell mass that could be exploited as novel therapies for patients with diabetes.

Publication types

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

MeSH terms

  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Body Composition / physiology
  • Cell Differentiation / physiology
  • Corticosterone / blood
  • Eating / physiology*
  • Female
  • Fetal Growth Retardation / metabolism
  • Fetal Growth Retardation / physiopathology
  • Glucocorticoids / metabolism*
  • Glucose Tolerance Test
  • Humans
  • Insulin / metabolism
  • Insulin-Secreting Cells / metabolism*
  • Islets of Langerhans / metabolism
  • Male
  • Mice
  • Nerve Tissue Proteins / metabolism
  • Polymerase Chain Reaction
  • Pregnancy
  • Receptors, Glucocorticoid / genetics
  • Receptors, Glucocorticoid / metabolism*


  • Basic Helix-Loop-Helix Transcription Factors
  • Glucocorticoids
  • Insulin
  • NEUROG3 protein, human
  • Nerve Tissue Proteins
  • Receptors, Glucocorticoid
  • Corticosterone