Peer Reviewed

1

Document Type

Article

Publication Date

2016

Keywords

Appetite Control, Obesity

Funder/Sponsor

RCSI Alumni

Comments

This article is also available at http://www.rcsismj.com/rcsismj-volume-9-2015-2016/

Abstract

Traditionally, obesity has been viewed as a simple disease of excess calorific intake in the context of a sedentary lifestyle. However, while an increase in energy consumption without corresponding expenditure is a key force in the initial development of obesity, a number of homeostatic mechanisms conspire to maintain high adiposity in individuals who are already overweight. Both central neuronal mechanisms and peripheral endocrine signals drive increased appetite and reduced metabolic rate in the obese. This prevents weight loss from occurring as quickly as one would expect, and makes sustained weight loss of more than 15% almost impossible. Currently, the most effective therapy for obesity is bariatric surgery. While previously believed to effect weight loss through malabsorption, restriction of stomach capacity or both, it is now shown that these operations fundamentally change the internal milieu of obese individuals, favouring weight loss and a reduction in appetite via cumulative changes in neuroendocrine signalling. This has led to some exploration of methods to directly affect the final common pathways in the brain and more efficiently produce weight loss.

Disciplines

Medicine and Health Sciences

Citation

O'Reilly D. I eat, therefore I am: the gut-brain axis and appetite control. RCSI Student Medical Journal. 2016;9(1):62-64.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 License.

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