A new piece of the diabetes puzzle

Since the 1990s, researchers have struggled to explain how leptin, an enzyme that monitors how much energy our bodies generate, lowers high blood glucose in diabetic mice. Understanding this mechanism, they’ve known, could pave the way for new therapies for patients with type 1 and type 2 diabetes (T1D and T2D).

In the July 2014 issue of Nature Medicine, members of the lab of Gerald I. Shulman, M.D., Ph.D., George R. Cowgill Professor of Medicine, reported on a mechanism by which leptin mediates its action. The team observed that fasting T1D and T2D mice had low levels of leptin, and increasing leptin levels reversed hyperglycemia. They found that leptin inhibits the hypothalamic-pituitary-adrenal (HPA) axis, a critical neuroendocrine pathway that regulates body processes such as stress response.

The results suggest “leptin could be an additional therapy [with insulin] that could vastly improve blood glucose control” in diabetics, says lead author Rachel J. Perry, Ph.D., postdoctoral fellow in medicine.


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