A long-standing puzzle in the diabetes field has been the fact that only a small subset of insulin-producing beta cells in the pancreas of adult organisms can replicate (and, hence, contribute to beta cell regeneration in diabetes). Furthermore, this subset of replicating cells continues to decline with advancing age. Young animals demonstrate a superb potential for tissue regeneration. Because this tissue regeneration deteriorates with age, it is generally assumed that the younger the animal, the better it compensates for tissue damage. In a new study published in Developmental Cell, Professor Yuval Dor and research associate Dr. Miri Stolovich-Rain at the Hebrew University of Jerusalem’s Institute for Medical Research Israel-Canada (IMRIC), in collaboration with Professor Benjamin Glaser from the Hadassah Medical Center, set out to understand the age-related decline of beta cell regeneration. To do this, they examined the ability of beta cells in young mice to replicate in response to hyperglycemia, a condition in which excessive glucose circulates in the blood. Expecting to find a superb regenerative response that declines with age, the researchers were surprised to discover that young mice don’t begin to possess the cellular machinery that allows them to regenerate after they are done weaning. Examining the production of pancreatic beta cells in suckling mice, the researchers found that in these young mice, beta cells failed to enter the cell division cycle in response to high levels of glucose. In addition, insulin secretion in response to high levels of glucose was much reduced compared with the situation in adult mice.
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