PMID- 23636998 OWN - NLM STAT- MEDLINE DCOM- 20140331 LR - 20211103 IS - 1708-0428 (Electronic) IS - 0960-8923 (Linking) VI - 23 IP - 9 DP - 2013 Sep TI - Duodenal-jejunal bypass improves glucose metabolism and adipokine expression independently of weight loss in a diabetic rat model. PG - 1436-44 LID - 10.1007/s11695-013-0976-1 [doi] AB - BACKGROUND: There is accumulating evidence that adipokines lead to a proinflammatory state, which plays crucial roles in insulin resistance and development of type 2 diabetes mellitus (T2DM). Previous studies demonstrated that weight loss after bariatric surgery is accompanied by a suppression of the proinflammatory state. However, the effect of bariatric surgery on adipokine expression beyond weight loss is still elusive. The aim of this study was to investigate the effect of duodenal-jejunal bypass (DJB) on glucose homeostasis and adipokine expression independently of weight loss. METHODS: A T2DM rat model was developed by a high-fat diet and low dose of streptozotocin. Twenty-one diabetic rats and 10 age-matched SD rats were randomly assigned to the DJB group, sham-DJB (S-DJB) group, and control group. For 12 weeks after surgery, their body weight, food intake, glucose homeostasis, lipid parameters, serum adipokine levels, and adipokine gene expression in the mesocolon adipose tissue were measured. RESULTS: Compared to the S-DJB group, DJB induced significant and sustained glycemic control with improved insulin sensitivity and glucose tolerance independently of weight loss. DJB improved the lipid metabolism by decreasing fasting free fatty acids and triglycerides. Serum leptin and IL-6 significantly decreased 12 weeks after DJB, whereas adiponectin increased and TNF-alpha remained unchanged. The mRNA expression levels of leptin, TNF-alpha, and IL-6 decreased, whereas adiponectin increased in the mesocolon adipose tissue. CONCLUSION: DJB reduced the proinflammatory adipokines and increased the anti-inflammatory adipokines independently of weight loss, which may contribute to the improvement of insulin sensitivity. FAU - Hu, Chunxiao AU - Hu C AD - Department of General Surgery, Qilu Hospital of Shandong University, 107#, Wenhua Xi Road, Jinan 250012, Shandong, PR China. FAU - Zhang, Guangyong AU - Zhang G FAU - Sun, Dong AU - Sun D FAU - Han, Haifeng AU - Han H FAU - Hu, Sanyuan AU - Hu S LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Obes Surg JT - Obesity surgery JID - 9106714 RN - 0 (Adiponectin) RN - 0 (Blood Glucose) RN - 0 (Interleukin-6) RN - 0 (Tumor Necrosis Factor-alpha) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Adiponectin/metabolism MH - Adipose Tissue/immunology/*metabolism MH - Animals MH - Blood Glucose/metabolism MH - Body Weight MH - Diabetes Mellitus, Experimental/metabolism MH - Diabetes Mellitus, Type 2/immunology/*metabolism/*surgery MH - Duodenum/metabolism/*surgery MH - Eating MH - *Gastric Bypass MH - Gene Expression Regulation MH - Glucose/*metabolism MH - Homeostasis MH - Insulin Resistance MH - Interleukin-6/metabolism MH - Jejunum/metabolism/*surgery MH - Male MH - Rats MH - Rats, Sprague-Dawley MH - Tumor Necrosis Factor-alpha/metabolism MH - Weight Loss/immunology EDAT- 2013/05/03 06:00 MHDA- 2014/04/01 06:00 CRDT- 2013/05/03 06:00 PHST- 2013/05/03 06:00 [entrez] PHST- 2013/05/03 06:00 [pubmed] PHST- 2014/04/01 06:00 [medline] AID - 10.1007/s11695-013-0976-1 [doi] PST - ppublish SO - Obes Surg. 2013 Sep;23(9):1436-44. doi: 10.1007/s11695-013-0976-1.