SUN-113 Adipocyte Morphology And Cytokine Gene Expression In Adipose Tissue From Patients Before And After Weight Loss From Bariatric Surgery

Multiple studies have implicated the accumulation of adipose tissue macrophages (ATMs) in the inflammatory response in obesity. In particular, increased secretion of pro-inflammatory cytokines is thought to cause local and systemic insulin resistance in a paracrine/endocrine fashion and is associated with obesity. It has been shown that ATMs accumulate in adipose tissue of obese individuals and increase in number with increasing mass. Yet, fasting also causes increased ATM accumulation. Numerous studies have shown that bariatric surgery reduces insulin resistance, cardiovascular disease and mortality independent of weight loss, effects thought to be related to the reduction in inflammation seen after bariatric surgery. However, the finding that pro-inflammatory gene expression decreases after human weight loss has been inconsistent across multiple studies. Here we have analyzed adipose tissue biopsies from five patients before and after undergoing sleeve gastrectomy to determine adipocyte morphology, pro-inflammatory cytokine gene expression, and macrophage infiltration of adipose tissue before and after weight loss. Levels of gene expression of pro-inflammatory markers IL-6, IL-1β and TNFα from subcutaneous adipose tissue were not significantly different in subjects before and three months after undergoing bariatric surgery despite significant weight loss in all subjects. Furthermore, gene expression levels of IL-10, an anti-inflammatory cytokine did not change after weight loss. Adipocyte morphology studies showed that adipocyte size appears to decrease after weight loss which is consistent with other studies. However, macrophage infiltration by immunofluorescence persisted in adipose tissue after bariatric surgery despite improved insulin sensitivity in these tissues and weight loss. These results indicate that macrophages are not only associated with the pro-inflammatory or obese state but they may play a distinct role in the setting of obesity and also in the setting of sustained weight loss. Thus, their classification as either pro-inflammatory “M1” or anti- inflammatory “M2” may not fully capture their heterogeneity or the scope of their metabolic function. Detailed studies looking at the activation state or metabolic phenotype of infiltrating macrophages before and after weight loss are needed. Our studies will provide insights into the role of inflammatory mediators after weight loss, in particular the metabolic role of the macrophage in during obesity and after extreme weight loss.