Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats
Yi Shen, Yang Liu, Shao-Qiu Zheng, Jiang Han, Er-Li Pei, Zhi-Hong Li, Xiao-Yun Xie, Zhi-Qiang Li, Ming Luo
Department of Geriatrics, Tongji Hospital, Tongji University, School of Medicine, Shanghai, China (mainland)
Med Sci Monit 2019; 25:6719-6726
DOI: 10.12659/MSM.915532
Available online: 2019-09-07
Published: 2019-09-07

BACKGROUND:
Bariatric procedures such as left gastric artery ligation (LGAL) and sleeve gastrectomy (SG) have emerged as important procedures for treating morbid obesity. In this study, we compared the effects of LGAL vs. SG on obesity-induced adipose tissue macrophage infiltration and inflammation in diet-induced obese rats.
MATERIAL AND METHODS:
Sprague-Dawley (SD) rats were fed a high-fat diet (HFD) for 16 weeks to induce obesity. SG, GLAL, or corresponding sham surgeries were performed in anesthetized rats. Inflammatory factor expression in serum and epididymal and retroperitoneal adipose tissues were analyzed 4 weeks after surgery. Macrophage infiltration and phenotype transformation were also assessed with Western blot analysis and immunofluorescence.
RESULTS:
Both LGAL and SG strongly attenuated high-fat diet (HFD)-induced fat accumulation in retroperitoneal and epididymal tissues. The expressions of inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 were downregulated after LGAL and after SG by promoting activation of M2 macrophages, despite continued exposure to HFD. Furthermore, both LGAL and SG resulted in increased macrophage infiltration, but did not contribute to phenotype transformation of macrophages to M1.
CONCLUSIONS:
LGAL and SG both reduced fat accumulation caused by HFD feeding. Therapies designed to ameliorate the inflammatory response by promoting activation of M2 macrophages may be valuable.
Keywords: Bariatric Surgery, Diabetes Mellitus, Type 2, Insulin Resistance, Macrophages, Obesity, Morbid