Does bariatric surgery improve adipose tissue function?

Abstract

Summary Bariatric surgery is currently the most effective treatment for obesity. Not only do these types of surgeries produce significant weight loss but also they improve insulin sensitivity and whole body metabolic function. The aim of this review is to explore how altered physiology of adipose tissue may contribute to the potent metabolic effects of some of these procedures. This includes specific effects on various fat depots, the function of individual adipocytes and the interaction between adipose tissue and other key metabolic tissues. Besides a dramatic loss of fat mass, bariatric surgery shifts the distribution of fat from visceral to the subcutaneous compartment favoring metabolic improvement. The sensitivity towards lipolysis controlled by insulin and catecholamines is improved, adipokine secretion is altered and local adipose inflammation as well as systemic inflammatory markers decreases. Some of these changes have been shown to be weight loss independent, and novel hypothesis for these effects includes include changes in bile acid metabolism, gut microbiota and central regulation of metabolism. In conclusion bariatric surgery is capable of improving aspects of adipose tissue function and do so in some cases in ways that are not entirely explained by the potent effect of surgery.

Macrophage Proliferation Sustains Adipose Tissue Inflammation in Formerly Obese Mice

“…Clinical studies have shown a persistent risk for cardiometabolic disease in formerly obese adults (17,21,45). Our study suggests that obesity elicits damage responses in AT that persist despite WL and that may contribute to this risk.…”

“…We posit that maintenance of these features within AT, particularly inflammation, could contribute to the persistence of metabolic disease risk observed in formerly obese patients. It will be critical to compare our results using dietary manipulation with the induction of WL by other mechanisms such as bariatric surgery, which may impart different outputs in the inflammatory state of AT (45). A potential weaknesses of this study is that our WL protocol did not use isocaloric diets and did not control for food intake by pair feeding.…”

Adipose tissue: between the extremes

“…Thus, macrophage infiltration of adipose tissue was a strong predictor of insulin resistance in obese subjects after matching for BMI and other factors (Klö ting et al, 2010). Similarly, one of the effects of bariatric surgery is the reduction of macrophage infiltration in conjunction with insulin sensitization (Frikke-Schmidt et al, 2016). The causal relationship between obesity-induced chronic inflammation and metabolic dysfunction has been established in numerous mouse models with genetic manipulation of key inflammatory pathways [reviewed in (Lackey & Olefsky, 2016)].…”

Bile acids and bariatric surgery

“…Through kinase signaling pathways, TGR5 activation stimulates gallbladder filling (T. Li et al, 2011), modulates energy expenditure (Watanabe et al, 2006), stimulates GLP-1 release from intestinal L cells (Habib et al, 2013; Katsuma et al, 2005; Thomas et al, 2009), suppresses hepatic glycogenolysis (Potthoff et al, 2013) reduces inflammation (Frikke Schmidt et al, 2016) and inflammatory macrophage activation (Kawamata et al, 2003; Keitel et al, 2008; Lou et al, 2014; Maruyama et al, 2002; Y. D. Wang et al, 2008), improves pancreatic function (Kumar et al, 2016; Vettorazzi et al, 2016) and improves non-alcoholic fatty liver disease (Ding et al, 2016).…”