Bariatric surgery is undoubtedly the most effective treatment for morbid obesity. It has also proven to be a boon for obesity-related co-morbidities, especially, type 2 diabetes as many patients achieve remission of diabetes after bariatric surgery. But how does bariatric surgery work? Most people understand that bariatric surgery works by reducing food intake alone, but there are many role mechanisms which play crucial roles both in weight loss as well as improvement of associated diseases like type 2 diabetes. These mechanisms include a reduction in food absorption, increase in energy expenditure, eating behavior changes, various intestinal hormonal alterations and changes in adipocytokines (cell signaling proteins produced by fat cells) like Leptin, Adiponectin, and Omentin.

Today we will talk about the adipocytokine Leptin and its bit in the puzzle of bariatric surgery. Leptin is secreted by white fat tissue of the body, and it plays an important role in energy balance. What has been found about leptin in non-obese individuals is that high leptin levels are associated with satiety and low leptin levels are associated with hunger. However, it is striking to find that obese individuals tend to have high leptin levels. This has brought us to understand that obese individuals have leptin resistance, similar to insulin resistance, and thus, they have increased hunger and reduced energy expenditure in spite of high leptin levels. After bariatric surgery, leptin levels fall as weight loss progresses, and so does the leptin resistance. Changes in leptin levels after bariatric surgery is a clear example of the complex interplay for various chemicals contributing to the benefits of bariatric surgery.