TUESDAY, Sept. 4 (HealthDay News) -- The function of special glucose-sensing neurons in the hypothalamus is impaired by obesity, suggesting these cells have a role in the pathogenesis of type 2 diabetes, according to a study published online Aug. 29 in Nature.
Laura E. Parton, M.D., of Beth Israel Deaconess Medical Center and Harvard Medical School in Boston, and colleagues investigated the role that glucose-sensing pro-opiomelanocortin (POMC) neurons have in the regulation of blood glucose and the development of type 2 diabetes.
The researchers showed that mice expressing a mutant protein that interfered with glucose-sensing in POMC neurons exhibited an impaired whole-body response to a systemic glucose load, suggesting that these glucose-sensing neurons help regulate blood glucose. The scientists also showed that the neurons of mice who were fed a high-fat diet lost glucose-sensing ability when they became obese.
The mechanism for obesity-induced loss of glucose sensing is attributed to uncoupling protein 2 (UCP2), a mitochondrial protein. This protein has been shown to inhibit glucose sensing in the POMC. The neurons of mice deficient in UCP2 did not lose glucose-sensing ability when the mice became obese. In addition, pharmacologic inhibition of UCP2 protected glucose sensing in neurons.
"Obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited neurons might have a pathogenic role in the development of type 2 diabetes," the authors conclude.
Abstract
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