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Treatments for obesity: view from the Chair

International Journal of Obesity volume 33, pages S22–S23 (2009)Cite this article

The control of body weight involves a complex interplay between a variety of factors. Genetics, culture, environment, mood, and the types and tastes of foods around us all can influence our body weight and adiposity. This complexity is not itself a problem, but problems arise when adiposity increases beyond a limit and we must identify a specific cause for obesity. Reducing body weight permanently is far more difficult for most overweight people than it is to gain weight in the first place. Thus, reports on hormones that regulate appetite or on bariatric surgical procedures with unexpected endocrine benefits are greeted with great interest. This review focuses on two papers that deal with such issues.

The first report,1 by Thomas Lutz, centers on the hormone amylin. Amylin is released by the same pancreatic beta cells that release insulin, and acts in concert with insulin in response to elevated blood glucose to optimize energy balance by reducing food intake, slowing gastric emptying and suppressing secretion of glucagon after a meal.2, 3 These coordinated actions seem to be mediated by actions in the brain, beginning with the area postrema,3, 4 and then to the forebrain and lateral hypothalamus.3 Similar to many other centrally active hormones,5 injection of amylin into the brain results in reduced food intake and body weight, independent of the body weight at the start of treatment. Also, similar to the melanocortin peptides,5 acute administration of the amylin agonist, salmon calcitonin, centrally results in reduced energy expenditure. Interestingly, animals overfed for 3 weeks with an energy-dense diet were resistant to amylin's effect on body weight. Thus, although amylin receptors might serve as useful targets in the battle against overweight, there might be limitations to their regulatory actions precisely in the populations that are the target for the potential therapeutic use of amylin, which is not dissimilar to the results of even moderate fat diets in obesity-prone rats suppressing responses to anorexigenic hormones like leptin or melanocortins.6 Despite this, the numerous physiological regulators of meal size and energy expenditure, such as amylin, that have emerged over the past few years certainly provide an array of therapeutic targets for the treatment of obesity.

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Acknowledgements

WF Colmers is a Medical Scientist of the Alberta Heritage Foundation for Medical Research. Work in his laboratory is supported by the Canadian Institutes for Health Research.

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  1. Department of Pharmacology, University of Alberta, Edmonton, Alberta, Canada

    W F Colmers

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Colmers, W. Treatments for obesity: view from the Chair. Int J Obes 33 (Suppl 1), S22–S23 (2009). https://doi.org/10.1038/ijo.2009.12

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