Bariatric Surgery and T2D

Overall, bariatric surgery results in the remission of T2D in up to 84% of patients. Although BPD is most effective at facilitating remission of T2D, this procedure is also associated with a worse adverse event rate post‐surgery than other bariatric procedures. Factors additional to weight loss following bariatric surgery likely contribute to improvements in insulin resistance and subsequent remission of T2D. Accordingly, improvements in blood glucose levels in T2D usually occur within just a few days of the bariatric surgical procedure and prior to any observed weight loss. Factors that drive the remission of T2D following bariatric surgery may relate to anatomical remodelling of the gastrointestinal tract that occur with some forms of the procedure. These include alterations to (i) hormonal regulation, (ii) cellular processes and (iii) the gut microbiome. Here, we outline evidence to support each of these processes (summarised in Figure 21.1).

Alterations to hormonal regulation: Glucagon‐like peptide 1 (GLP‐1) is an incretin hormone that improves insulin sensitivity, enhances pancreatic release of insulin, suppresses pancreatic release of glucagon, suppresses appetite and slows gastric emptying in the post‐prandial period. Compared with pre‐surgery, serum levels of GLP‐1 increases in the post‐prandial period following bariatric surgery. Furthermore, in post‐bariatric surgery patients, post‐prandial serum GLP‐1 levels correlate directly with improvements in measures of glycaemic control.

Acting in concert with GLP‐1, a further incretin hormone, gastro‐inhibitory peptide (GIP), also enhances pancreatic release of insulin in response to eating. GIP may also affect satiety. In contrast to GLP‐1, GIP enhances post‐prandial glucagon response. There is controversy in the literature regarding the effects of bariatric surgery on post‐prandial serum levels of GIP, with some studies showing an increase, some showing a decrease and others showing no difference compared with pre‐surgical levels. Based on these conflicting reports, it is therefore not clear what are the effects of bariatric surgery on post‐prandial serum GIP. A potential role for GIP in the improvement and remission of T2D following bariatric surgery remains tenuous based on current evidence.

The incretin hormones GLP‐1 and GIP exert their effects within the post‐prandial period. Such effects include appetite regulation. In contrast, ghrelin exerts its effects mainly before a meal, as a key stimulator of enhanced appetite and hunger. Ghrelin therefore drives food intake and affects the regulation of body weight. Some studies have shown a reduction in levels of fasting serum ghrelin following bariatric surgery.

Other possible alterations to hormonal regulation following bariatric surgery include changes in serum glucagon (action of which opposes that of insulin). There is controversy in the literature regarding changes in post‐prandial serum glucagon levels following bariatric surgery, with some studies showing a reduction and others showing no significant change. Therefore, a possible role for changes in glucagon as a mediator of T2D resolution following bariatric surgery remains unclear. Finally, changes in bile acid circulation following bariatric surgery may improve insulin sensitivity and remission of T2D. Bile acids stimulate the release of incretin hormones from the intestinal L‐cells, including GLP‐1, peptide YY (PYY) and oxyntomodulin. Through such effects, increased levels of bile acids could improve post‐prandial insulin release and satiety, and contribute to remission of T2D following bariatric surgery. However, this mechanism remains speculative and requires further study to confirm or refute such a hypothesis.

Alterations to cellular processes: One of the benefits of bariatric surgery is a reduction in fat content of both the liver and pancreas. Reduced hepatic and pancreatic fat content associate with improved hepatic cellular insulin sensitivity and glucose uptake, and improved beta cell insulin release, respectively. Improved hepatic insulin sensitivity and pancreatic beta cell insulin release both likely contribute to the remission of T2D post‐bariatric surgery. Reduced inflammation may mediate the cellular mechanisms by which reduced hepatic and pancreatic fat content improve metabolic function post‐bariatric surgery. Such dampening of inflammatory response may result in changes to expression of mRNA in such a way that improves glycaemic control.

Alterations to the gut microbiome: There are 100 trillion microbes in the human digestive tract. Certain microbial species, such as Anaerococcus, Corpococcus, Fusobacterium and Parvimonas associate with obesity. Other microbial species, such as Akkermansia muciniphila, Enterococcus and bacteria producing short chain fatty acids associate with a healthy body weight. It is clear from the literature that following bariatric surgery, characteristic changes occur in the gut microbiome. Such changes appear to be procedure‐specific. For example, the microbial species Bacteroides thetaiotaomicron characteristically increases proportionately following LSG, and the microbial species Proteobacteria

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