Longevity of human islet α- and β-cells

Diabetes Obes Metab. 2011 Oct;13 Suppl 1:39-46. doi: 10.1111/j.1463-1326.2011.01443.x.


Pancreatic islet cell regeneration is considered to be important in the onset and progression of diabetes and as a potential cell therapy. Current hypotheses, largely based on rodent studies, indicate continuous turnover and plasticity of α- and β-cells in adults; cell populations in rodents respond to increased secretory demand in obesity (30-fold β-cell increase) and pregnancy. Turnover and plasticity of islet cells decrease in mice within >1 year. In man, morphometric observations on postmortem pancreas have indicated that the cellular expansion is much smaller than the increased insulin secretion that accompanies obesity. Longevity of β-cells in humans >20-30 years has been shown by (14) C measurements and bromo-deoxyuridine (BrdU) incorporation and there is an age-related decline in the expression of proteins associated with cell division and regeneration including cyclin D3 and PDX-1. Quantitative estimation and mathematical modelling of the longevity marker, cellular lipofuscin body content, in islets of subjects aged 1-84 years indicated an age-related increase and that 97% of the human β-cell population was established by the age of 20. New data show that human α-cell lipofuscin content is less than that seen in β-cells, but the age-related accumulation is similar; lipofuscin-positive (aged) cells form ≥ 95% of the population after 20 years. Increased turnover of cellular organelles such as mitochondria and endoplasmic reticulum could contribute to lipofuscin accumulation with age in long-lived cells. Induction of regeneration of human islet cells will require understanding of the mechanisms associated with age-related senescence.

Publication types

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

MeSH terms

  • Age Factors
  • Aging / physiology*
  • Animals
  • Apoptosis
  • Blood Glucose / metabolism
  • Cell Division
  • Diabetes Mellitus, Type 2 / genetics
  • Diabetes Mellitus, Type 2 / metabolism*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Glucagon-Secreting Cells / metabolism
  • Glucagon-Secreting Cells / physiology*
  • Humans
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / physiology*
  • Lipofuscin / metabolism*
  • Mice


  • Blood Glucose
  • Lipofuscin