I eat, therefore I am: the gut-brain axis and appetite control
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.
CommentsThis article is also available at http://www.rcsismj.com Part of the RCSIsmj collection: https://doi.org/10.25419/rcsi.c.6775842.v1
Published CitationO'Reilly D. I eat, therefore I am: the gut-brain axis and appetite control. RCSIsmj 2016;9(1):62-64.
- Undergraduate Research
PublisherRCSI University of Medicine and Health Sciences
- Published Version (Version of Record)