The Benefits Of Bariatric Surgery

Obesity is increasing in prevalence and is associated with many non-communicable diseases including: stroke, type II diabetes, non-alcoholic fatty liver disease, coronary heart disease, cancer, and other adverse health states. As prevalence of obesity increases, the popularity of bariatric surgery also rises for treatment in obesity by achieving and managing long-term weight loss while decreasing health risks. (A, p 1-2)(B, p 2)(C, p 2). The most common type of bariatric surgery performed is the Roux-en-Y gastric bypass surgery. The procedure drastically decreases stomach volume and bypasses the duodenum by attaching the stomach to the jejunum. (A, p 3-4) (B, p 2). Roux-en-Y bypass surgery promotes weight loss through decreased food intake due to the decreased size of the stomach and by malabsorption as each part of the small intestine has specific roles in digestion, mixing and stimulation of enzymes, and absorptive properties. Bariatric surgeries are successful due to caloric restriction from stomach volume limitations and malabsorption, adjusting movement of food through the GI tract, and anatomical rearrangement causing a change in gut hormone secretion. Initial changes in blood glucose regulation, appetite management, and weight loss are due to physiological changes in the digestive process and circulating levels of gut-hormones including: leptin, GLP-1, Peptide YY, and Ghrelin (A, p 3-9) (B, p 2-3) (D, p 1085). Bariatric surgery goes beyond the sole promotion of weight loss by reducing obesity related comorbidities, so is better characterized as a metabolic surgery (A, p 2) (C, p 2). Leptin levels are decreased following bariatric surgery. Leptin is a hormone primarily produced by adipocytes, which promotes satiety and regulates energy balance by signaling the neural pathways in the hypothalamus to activate pro-opiomelanocortin (POMC) neural pathways or agouti-related peptide (NPY) neural pathways. The neural pathways secrete neurotransmitters, which increase or decrease appetite and regulate energy expenditure for adaptive energy homeostasis (B, p 3) (F, p 2-3). Leptin levels are regulated by the amount of adipose tissue present, so procedures decreasing adipose tissue such as bariatric surgery will decrease leptin concentrations. Interestingly, fasted leptin concentrations decreased after only a couple of weeks post-surgery before a significant amount of adipose tissue is lost suggesting the procedure directly influences lepin levels. Leptin levels decrease quickly after bariatric surgery because leptin is secreted in the stomach, which is considerably reduced (B, p 3-7). GLP-1 and PYY are two anorexogenic gut hormones, secreted by L cells of the ileum and colon that slow gastric emptying, promote insulin release, and inhibit acid secretion in the stomach. …show more content…
(B, p 2) (C, p 2). Post-prandial GLP-1 and PYY levels increase after bariatric surgery, due to a greater stimulation of the L-cells in the distal intestine from an increase in unabsorbed nutrients. Increase in these levels amplifies the feeling of satiety and can further contribute to weight loss (C, p 2). Bariatric surgery decreases fasting hunger rating (analyzed using the visual analog scale), specifically after a balanced nutrient meal (Total calories: protein 32%, carbs 47%, fat 21%), following surgery (53.3 +/- 11.6 mm verses 25.4 +/- 7.8 mm) indicating the decrease in hunger is due to satiety promoted by increased levels of GLP-1 and PYY (C, p 3&5). Secretion of GLP-1 occurs in response to gastric emptying and is dependent on the size of the meal and nutrient composition. Fat, protein, glucose, and lipids are all stimuli for GLP-1 release with lipids having an exaggerated response (D, p 1085). Once L-cells in the distal gut are stimulated by nutrients present, GLP-1 is released and acts by slowing transit through the gastrointestinal tract thus promoting a feeling of satiety (A, p 6). GLP-1 levels, once increased, can remain elevated many hours after initial increase to provide prolonged benefits in hunger regulation leading to decrease dietary intake and …show more content…
Active PYY binds to receptors on the NPY neural pathway and inhibits the release of neurotransmitters, which promotes increased appetite (A, p 8). Post-prandial and total PYY levels increase post-procedure (post prandial p<0.05). Protein provides the greatest increase in satiety when compared to carbohydrates and fats, so this could contribute to the differing results as ghrelin levels decreases in the presence of food in the digestive tract (B, p 9). Research procedures differ drastically and may contribute to the controversial results (B, p 8 &