MONDAY, Oct. 19 (HealthDay News) -- Mice deficient in a gastrointestinal hormone implicated in glucose metabolism spontaneously develop impaired glucose tolerance, insulin resistance and visceral obesity, according to a study published online Oct. 9 in Endocrinology.
Noting that dipeptidyl peptidases (DPPs) such as DPP4 have been shown to cleave and inactivate gastrointestinal hormones such as glucagon-like peptide 1 that respond to changes in blood glucose levels, Olga V. Danilova, M.D., from Tufts University School of Medicine in Boston, and colleagues generated mice lacking neurogenin 3-specific DPP2 to assess the role of this protease in glucose metabolism.
The researchers found that the mice had normal levels of active glucagon-like peptide 1. By four months, the mice spontaneously developed fasting hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and visceral obesity. The mice also had higher food consumption, with increased adipose tissue mass and liver steatosis, but no change in weight and a higher respiratory exchange rate were noted. These effects worsened with increasing age or a high-fat diet.
"We report, for the first time, that DPP2 enzyme activity is essential for preventing hyperinsulinemia and maintaining glucose homeostasis," Danilova and colleagues conclude. "Interestingly, the phenotype of NGN3-DPP2 knockdown mice is opposite that of DPP4 knockout mice with regard to glucose metabolism, namely the former have normal glucagon-like peptide 1 levels but present with glucose intolerance, whereas the latter have increased glucagon-like peptide 1, which is accompanied by augmented glucose tolerance."
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