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Longevity of human islet α- and β-cells
M Cnop1, M Igoillo-Esteve, S J Hughes
1Laboratory of Experimental Medicine, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Diabetes, Obesity & Metabolism
|August 10, 2011
Summary
Human islet cells, crucial for diabetes and cell therapy, show limited regeneration after age 20. Understanding age-related senescence is key to inducing islet cell regeneration.
Area of Science:
- Endocrinology
- Cell Biology
- Regenerative Medicine
Background:
- Pancreatic islet cell regeneration is vital for diabetes onset, progression, and cell therapy.
- Rodent studies suggest continuous α- and β-cell turnover and plasticity, responding to metabolic demands.
- Human islet cell plasticity appears limited compared to rodents, with reduced regenerative capacity in aging.
Purpose of the Study:
- To investigate the plasticity and longevity of human pancreatic islet cells (α- and β-cells) in relation to aging.
- To understand the mechanisms underlying the age-related decline in islet cell regeneration.
- To identify factors hindering the induction of human islet cell regeneration for therapeutic purposes.
Main Methods:
- Analysis of morphometric data from postmortem human pancreases.
- Measurement of β-cell longevity using carbon-14 ((14)C) dating and bromo-deoxyuridine (BrdU) incorporation.
- Quantitative estimation and mathematical modeling of cellular lipofuscin body content in human islets across a wide age range (1-84 years).
- Assessment of age-related changes in proteins associated with cell division (e.g., cyclin D3, PDX-1).
Main Results:
- Human β-cells have a longevity of over 20-30 years, with 97% of the population established by age 20.
- Age-related decline in cell division and regeneration markers (cyclin D3, PDX-1) was observed.
- Lipofuscin accumulation, a marker of aging, increases with age in both α- and β-cells, with ≥95% of cells showing lipofuscin after 20 years.
- Human islet cell expansion in obesity is less pronounced than in rodents.
Conclusions:
- Human pancreatic islet cell populations are largely established by age 20 and exhibit limited plasticity and regeneration thereafter.
- Age-related senescence, potentially linked to organelle turnover (mitochondria, endoplasmic reticulum), limits human islet cell regenerative potential.
- Further research into age-related senescence mechanisms is necessary to develop strategies for inducing human islet cell regeneration for diabetes therapy.
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