Mechanism of diabetes control after metabolic surgery
Gastrointestinal metabolic surgery is becoming the most effective therapy for type 2 diabetes (T2D) in obese patients. Mechanism underlying the glycemic control of metabolic surgery is intriguing and has been heavily investigated but still not well defined. Multiple plausible mechanisms, rather than a single predominant mechanism, likely mediate the early and long-term glycemic control after metabolic surgery. This paper examines the proposed mechanism from published research findings. Bariatric surgery consisted of three parts of anatomical changes: (I) gastric restriction; (II) exclusion of duodenum and upper intestine; (III) rapid delivery of food to distal intestine or short common channel. These anatomical changes may induce a lot of physiologic and molecular changes helping in the resolution of T2D. The proposed mechanisms included calories restriction and weight loss, ghrelin, duodenum exclusion effect with gastro-intestinal (GI) tract nutrient sensing, rapid distal nutrient delivery with gut hormone response, changes in bile acid metabolism, and intestinal microbiome. These changes, acting through peripheral and central pathway, result in reduced hepatic glucose, increased tissue glucose uptake, improved insulin sensitivity, and enhanced B-cell function. Different procedures may provide different mechanism and help in identifying novel therapeutic targets.