Abstract
Obesity surgery remains the most effective treatment for obesity and its complications. Weight loss was initially attributed to decreased energy absorption from the gut but has since been linked to reduced appetitive behavior and potentially increased energy expenditure. Implicated mechanisms associating rearrangement of the gastrointestinal tract with these metabolic outcomes include central appetite control, release of gut peptides, change in microbiota, and bile acids. However, the exact combination and timing of signals remain largely unknown. In this review, we survey recent research investigating these mechanisms, and seek to provide insights on unanswered questions over how weight loss is achieved following bariatric surgery which may eventually lead to safer, nonsurgical weight-loss interventions or combinations of medications with surgery.
Highlights
Obesity surgery over the past six decades has been successful in providing a means of achieving substantial weight loss and in giving us many novel insights on the pathophysiology of obesity
Obesity surgery was first described in the 1960s, when it was observed that patients with sub-total gastrectomy for cancer lost t a considerable amount of weight 1
Several modifications to the technique led to the ip first laparoscopic gastric bypass in 1994 2, and the establishment of the three r techniques most widely-used in clinical practice today. sc The two main approaches that are currently performed widely are Roux-en-Y Gastric u Bypass (RYGB) and Vertical Sleeve Gastrectomy (VSG)
Summary
Obesity surgery over the past six decades has been successful in providing a means of achieving substantial weight loss and in giving us many novel insights on the pathophysiology of obesity. Measurement of meal-induced neuronal activation by means of c-Fos in obese mice showed that brainstem anorexia circuit may have a potential role in adaptive neural and behavioural changes involved in the strong early suppression of energy intake after RYGB 29 These findings from animal models support the observations from humans in that the direction of change in expression of neuropeptides in the hypothalamus and brainstem after RYGB and VSG is opposite to dieting and favour the maintenance of a lower body weight set point. As the extent to which energy expenditure drives weight reduction following obesity surgery remains unclear, the ability of bile acids to increase GLP-1 ted secretion 111 and the role of FGF19 on hypothalamic AgRP/NPY neurons 102 indicate an indirect anorectic effect as the main course of action after RYGB and VSG. Whether the strength Aand number of these associations is substantial enough to provide predictive power is unclear
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