title: Duodenal-jejunal bypass improves glucose metabolism and adipokine expression independently of weight loss in a diabetic rat model.
abstract: 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-α remained unchanged. The mRNA expression levels of leptin, TNF-α, and IL-6 decreased, whereas adiponectin increased in the mesocolon adipose tissue.
  
  
  CONCLUSIONS
  DJB reduced the proinflammatory adipokines and increased the anti-inflammatory adipokines independently of weight loss, which may contribute to the improvement of insulin sensitivity.
authors: Department of General Surgery, Qilu Hospital of Shandong University, 107#, Wenhua Xi Road, Jinan 250012, Shandong, PR China.
authors: Chunxiao
authors: C
authors: Hu
authors: Guangyong
authors: G
authors: Zhang
authors: Dong
authors: D
authors: Sun
authors: Haifeng
authors: H
authors: Han
authors: Sanyuan
authors: S
authors: Hu
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology / Q000378:metabolism* / Q000601:surgery*; D004386:Duodenum / Q000378:metabolism / Q000601:surgery*; D004435:Eating; D015390:Gastric Bypass; D005786:Gene Expression Regulation; D005947:Glucose / Q000378:metabolism*; D006706:Homeostasis; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000378:metabolism; D007583:Jejunum / Q000378:metabolism / Q000601:surgery*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015431:Weight Loss / Q000276:immunology
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose
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