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Animal models of bariatric/metabolic surgery shed light on the mechanisms of weight control and glucose homeostasis: view from the chair

Abstract

Bariatric/metabolic surgeries are remarkably effective in reducing weight over a sustained period of time, and they also have significant beneficial effects on glucose homeostasis. Interestingly, the metabolic benefits of these surgeries frequently occur before significant weight loss. Given these findings, it is perhaps not surprising that obesity researchers are asking, how does bariatric/metabolic surgery work? Establishing these mechanisms can offer new insights into the physiology of energy balance and the control of metabolism. In the second half of the 13th International Symposium of the Merck Frosst/CIHR Research Chair in Obesity, four papers that address the mechanisms of bariatric/metabolic surgery were presented. The papers that follow this viewpoint all make use of animal models to reveal the neurohumoral mechanisms underlying weight loss and improved glucose homeostasis after experimental bariatric surgery. The rodent models of the commonly used clinical procedures have shown that energy intake is increased, food reward is altered and that the proximal gut is important in the control of energy balance and glucose homeostasis. Taken together, these models shed light on the mechanisms of bariatric/metabolic surgery and offer new insights that, in the future, may lead to less invasive therapies.

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Acknowledgements

KAS is an Alberta Heritage Foundation for Medical Research Medical Scientist and the Crohn's and Colitis Foundation of Canada Chair in Inflammatory Bowel Disease Research at the University of Calgary. This paper is dedicated to a friend and colleague Henry S Koopmans who passed away on 17 April 2010.

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Correspondence to K A Sharkey.

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Sharkey, K. Animal models of bariatric/metabolic surgery shed light on the mechanisms of weight control and glucose homeostasis: view from the chair. Int J Obes 35 (Suppl 3), S31–S34 (2011). https://doi.org/10.1038/ijo.2011.145

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