title: Roux-en-Y esophagojejunostomy reduces serum and aortic inflammatory biomarkers in type 2 diabetic rats.
abstract: BACKGROUND
  Recent studies have shown the reduction in serum inflammatory biomarkers by bariatric surgery. However, few studies have reported its effects on local vascular inflammation. We have investigated the effects of Roux-en-Y esophagojejunostomy on both serum and aortic tissue inflammation biomarkers in type 2 diabetic rats.
  
  
  METHODS
  Sprague-Dawley rats were divided into five groups: diabetic RYEJ, diabetic RYEJ sham, diabetic food restriction, diabetic rats, and non-diabetic control (n = 6/group). At 4 weeks after surgery, serum leptin, interleukin-6, C-reactive protein, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), chemerin, and adiponectin were measured. Aortic expression of c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinases was examined with immunohistochemistry; aortic expression of IL-1β, TNF-α, intercellular adhesion molecule-1, and vascular adhesion molecule-1 was assessed with western blotting. Hyperinsulinemic-euglycemic clamps with tracer infusion were completed to assess insulin sensitivity.
  
  
  RESULTS
  Roux-en-Y esophagojejunostomy significantly decreased serum inflammatory parameters and increased the concentration of the anti-inflammatory mediator adiponectin. The aortic inflammatory protein expression was markedly decreased in the diabetic RYEJ group as compared with that of the diabetic group (P < 0.05). Additionally, Roux-en-Y esophagojejunostomy improved insulin sensitivity and dyslipidemia and decreased body weight and total body fat.
  
  
  CONCLUSIONS
  Roux-en-Y esophagojejunostomy reduces the systemic and local vascular inflammation. The improvements in systemic and vascular inflammation are not wholly dependent on the magnitude of weight loss. Moreover, Roux-en-Y esophagojejunostomy alleviates insulin resistance and improves the features of metabolic syndrome, leading to a reduction in multiple cardiovascular risks.
authors.affiliation: Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China, litong909@hotmail.com.
authors.forename: Bing
authors.initials: B
authors.lastname: He
authors.forename: Chong
authors.initials: C
authors.lastname: Yu
authors.forename: Runyu
authors.initials: R
authors.lastname: Du
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.forename: Ping
authors.initials: P
authors.lastname: Han
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology / Q000601:surgery*; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000473:pathology / Q000601:surgery*; D015390:Gastric Bypass; D007249:Inflammation / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015431:Weight Loss
chemical_list: D054392:Adipokines; D015415:Biomarkers; D015815:Cell Adhesion Molecules; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D020928:Mitogen-Activated Protein Kinases