Activation of cellular aging process could increase insulin secretion in diabetes patients

A cellular program that causes aging can also increase the production of insulin, which could have implications for understanding and treating diabetes, according to new research.
Scientists at the Hebrew University of Jerusalem investigated the activity of a gene named p16, which is known to activate a program called senescence in cells. Senescence prevents cells from dividing, and plays an important role in preventing cancer.
The activity of the p16 gene occurs in pancreatic beta cells during aging and limits the potential for cells to divide. This loss of function can lead to decreased insulin secretion and blood glucose levels subsequently becoming too high, increasing the risk of diabetes.
Before the study, the researchers were unaware as to how the p16 gene affected beta cell function. In studies on mice and humans, the effects of the p16 gene led to some surprising results.
In mouse studies, p16-induced cellular senescence was found to improve insulin secretion following glucose stimulatio, and beta cells actually started to function more efficiently. In diabetic mouse models, senescence actually led to improved glucose levels.
In human experiments, p16 was activated in islets, which also led to increased insulin secretion. This suggests that p16 is the main driver of enhanced insulin secretion following senescence in both humans and mice.
Study author Dr. Ittai Ben-Porath explained: “Senescence of cells is generally thought to represent a state in which cells lose their functionality, and contribute to tissue aging and disease. It was therefore very striking to observe that when beta cells enter this state during normal aging, the program allows them to function better, rather than worse.”
“The findings suggest that what we call aging is in fact a continuum, starting with a maturation process that actually improves the function of cells and tissue, at the expense of regenerative potential. This has important implications for how we think about beta cell function and dysfunction in diabetes,” added Dr. Ronny Helman.
The research could lead to a greater understanding of diabetes: specifically, how beta cell function and insulin secretion can be enhanced, and how certain drugs could activate senescence to improve diabetes treatment.
The findings were published in the journal Nature Medicine.

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