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High insulin levels tied to obesity pathway, new UT Southwestern research shows
Date:8/25/2014

UT Southwestern Medical Center researchers have identified a crucial link between high levels of insulin and pathways that lead to obesity, a finding that may have important implications when treating diabetes.

Researchers with the UT Southwestern's Touchstone Center for Diabetes found that giving mice high levels of insulin, which is typically done to counter the effects of diabetes or insulin resistance in Type 2 diabetes, also fosters processes that lead to obesity.

The discovery was made by studying mice engineered to lack receptors for a hormone called glucagon.

Glucagon spurs the liver's production of glucose into the bloodstream and thus maintains the fuel supply for the brain. Insulin blocks the secretion of glucagon, opposes glucagon action on the liver, and instructs the body to take up glucose from the blood. Type 2 diabetics cannot respond properly to insulin and have uncontrolled glucagon production, thereby causing their livers to overproduce glucose, contributing to high blood-sugar levels. Insulin is often given to people with type 2 diabetes to try to overcome insulin-resistance and lower the levels of glucose in the bloodstream.

But insulin also signals the body to produce fat, so when given the high levels of insulin needed to control excess glucose, mice become fat, explained corresponding author Dr. Michael Roth, Professor of Biochemistry at UT Southwestern and a member of the Touchstone Diabetes Center.

"We found that mice lacking the receptor for glucagon cannot get fat unless they are given the high levels of insulin found in mice (and humans) that have type 2 diabetes,"
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Contact: Russell Rian
russell.rian@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
Source:Eurekalert  

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