Hao Yu1, Zhigao Song2,3, Hongbin Zhang3, Kehong Zheng1, Junfang Zhan4, Qing Luo2, Jingbo Sun3, Li Liang2, Xiaojiang Dai5,6, Liangping Wu7,8,9. 1. Special Medical Service Center, Zhujiang Hospital of Southern Medical University, Guangzhou, 510280, China. 2. Southern Medical University, Guangzhou, 510515, China. 3. Department of Metabolic Surgery,, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, 510515, China. 4. Physical Examination Center, Guangzhou First People's Hospital, Guangzhou, 510000, China. 5. Department of Metabolic Surgery, UDM Medical Group, Guangzhou, 510515, China. drdaixj@163.com. 6. Abdominal surgery, Jinshazhou Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, 510515, China. drdaixj@163.com. 7. Southern Medical University, Guangzhou, 510515, China. drwulp@163.com. 8. Department of Metabolic Surgery, UDM Medical Group, Guangzhou, 510515, China. drwulp@163.com. 9. Abdominal surgery, Jinshazhou Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, 510515, China. drwulp@163.com.
Abstract
BACKGROUND: Current studies indicate that inflammation of white adipose tissue (WAT) is a pathogenic characteristic of insulin resistance. However, the significance of visceral WAT inflammation after bariatric surgery remains unclear. METHODS: Duodenojejunal bypass plus sleeve gastrectomy (DJB-SG) was performed on Goto-Kakisaki rats. Weight, fasting blood glucose (FBG), and homeostatic model assessment of insulin resistance (HOMA-IR) in the DJB-SG group were compared to those in a sham surgery (SHAM) group every 2 weeks. The results of an oral glucose tolerance test (OGTT) and the volume of visceral adipose tissue (Visc.Fat) were compared before and 8 weeks postsurgery. Eight weeks after surgery, the rats were sacrificed and visceral WAT collected from the greater omentum. Tumor necrosis factor-α (TNF-α) and cluster of differentiation 68 (CD68) expression in the WAT were evaluated in paraffin-embedded sections by immunohistochemistry. RESULTS: Compared with the SHAM group, the DJB-SG group demonstrated a significant reduction in weight, FBG, and HOMA-IR (P < 0.05), with elevation of insulin levels (P < 0.05) from 4 weeks after surgery. OGTT and the quantity of Visc.Fat were significantly reduced (P < 0.05) 8 weeks after surgery. Moreover, the expression of TNF-α and CD68 in the visceral white adipose tissue was significantly lower 8 weeks after surgery (P < 0.05). CONCLUSIONS: The DJB-SG model established in Goto-Kakisaki rats achieved anticipated efficacy. Reduced TNF-α-related inflammation in visceral WAT may result in improved insulin resistance.
BACKGROUND: Current studies indicate that inflammation of white adipose tissue (WAT) is a pathogenic characteristic of insulin resistance. However, the significance of visceral WAT inflammation after bariatric surgery remains unclear. METHODS: Duodenojejunal bypass plus sleeve gastrectomy (DJB-SG) was performed on Goto-Kakisaki rats. Weight, fasting blood glucose (FBG), and homeostatic model assessment of insulin resistance (HOMA-IR) in the DJB-SG group were compared to those in a sham surgery (SHAM) group every 2 weeks. The results of an oral glucose tolerance test (OGTT) and the volume of visceral adipose tissue (Visc.Fat) were compared before and 8 weeks postsurgery. Eight weeks after surgery, the rats were sacrificed and visceral WAT collected from the greater omentum. Tumor necrosis factor-α (TNF-α) and cluster of differentiation 68 (CD68) expression in the WAT were evaluated in paraffin-embedded sections by immunohistochemistry. RESULTS: Compared with the SHAM group, the DJB-SG group demonstrated a significant reduction in weight, FBG, and HOMA-IR (P < 0.05), with elevation of insulin levels (P < 0.05) from 4 weeks after surgery. OGTT and the quantity of Visc.Fat were significantly reduced (P < 0.05) 8 weeks after surgery. Moreover, the expression of TNF-α and CD68 in the visceral white adipose tissue was significantly lower 8 weeks after surgery (P < 0.05). CONCLUSIONS: The DJB-SG model established in Goto-Kakisaki rats achieved anticipated efficacy. Reduced TNF-α-related inflammation in visceral WAT may result in improved insulin resistance.
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