Chemical cholecystokinin receptor activation protects against obesity-diabetes in high fat fed mice and has sustainable beneficial effects in genetic ob/ob mice.

Irwin N, Montgomery IA, Moffett RC, Flatt PR.
Journal   Biochem Pharmacol.
Species  
Analytes Measured   Glucagon
Matrix Tested   Plasma
Year   2012
Volume  
Page Numbers  
Application   Metabolic
Abstract
The current study has determined the ability of (pGlu-Gln)-CCK-8 to counter the development of diet-induced obesity-diabetes and examined persistence of beneficial metabolic effects in high fat and ob/ob mice, respectively. Twice daily injection of (pGlu-Gln)-CCK-8 in normal mice transferred to a high fat diet reduced energy intake (p<0.001), body weight (p<0.01), circulating insulin and LDL-cholesterol (p<0.001) and improved insulin sensitivity (p<0.001) as well as oral and intraperitoneal (p<0.001) glucose tolerance. Energy intake, body weight, circulating insulin and glucose tolerance of (pGlu-Gln)-CCK-8 mice were similar to lean controls. In addition, (pGlu-Gln)-CCK-8 prevented the effect of high fat feeding on triacylglycerol accumulation in liver and muscle. Interestingly, (pGlu-Gln)-CCK-8 significantly (p<0.001) elevated pancreatic glucagon content. Histological examination of the pancreata of (pGlu-Gln)-CCK-8 mice revealed no changes in islet number or size, but there was increased turnover of beta-cells with significantly (p<0.001) increased numbers of peripherally located alpha-cells, co-expressing both glucagon and GLP-1. Beneficial metabolic effects were observed similarly in ob/ob mice treated twice daily with (pGlu-Gln)-CCK-8 for 18 days, including significantly reduced energy intake (p<0.05), body weight (p<0.05 to p<0.01), circulating glucose (p<0.05 to p<0.01) and insulin (p<0.05 to p<0.001) and improved glucose tolerance (p<0.05) and insulin sensitivity (p<0.001). Notably, these beneficial effects were still evident 18 days following cessation of treatment. These studies emphasize the potential of (pGlu-Gln)-CCK-8 for the treatment of obesity-diabetes.

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