Abstract
Aging and age-related diseases are associated with the impairment of tissue function and their regenerative capacity. In terms of pancreatic β-cells, it is well known that insulin resistance in peripheral tissues increases with age due to metabolic changes caused by adiposity or physical inactivity. But in the presence of functional β-cells, insulin resistance alone is insufficient to lead to type-2-diabetes. However, in combination with an insulin secretory dysfunction and a decreased β-cell mass coincided with advanced age, this leads to worsening of glucose tolerance and finally to hyperglycemia and the onset of type-2-diabetes. Investigations regarding the molecular basis of the limited proliferation capacity of aged endocrine pancreas revealed that cellular senescence seems to be involved. Senescence is characterized by an upregulation of tumor suppressor proteins such as p16Ink4a and p53, severe morphological diversifications or widespread changes in protein expression and secretion. But the impact of senescence-related changes on β-cell impairment has not yet been described. Therefore, by comparing lean C57Bl/6 J mice and adipose, diabetes-prone New Zealand Obese mice with diabetes-resistant B6.V-Lepob/J mice in different stages of age, we aim to characterize senescent β-cells and investigate the role of cellular senescence on β-cell functionality and proliferation.
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