title: Bariatric surgery reduces visceral adipose inflammation and improves endothelial function in type 2 diabetic mice.
abstract: OBJECTIVE
  Bariatric surgery is emerging as an effective method to alleviate a multitude of medical conditions associated with morbid obesity and type 2 diabetes. However, little is known about the effects and mechanisms of bariatric surgery on visceral fat inflammation and endothelial dysfunction in type 2 diabetes. We hypothesize that bariatric surgery ameliorates interferon-γ-mediated adipose tissue inflammation/oxidative stress and improves endothelial function in type 2 diabetic mice.
  
  
  RESULTS
  Control mice (m Lepr(db)) and diabetic mice (Lepr(db)) were treated with either sham surgery or improved gastric bypass surgery and then were evaluated at 5, 10, 20, and 30 days to assess postsurgical effects. Surgery reduced body weight, abdominal adiposity, blood glucose level, and food intake in Lepr(db). The surgery-induced decrease in visceral adiposity was accompanied by amelioration of T-lymphocytes and macrophage infiltration, as well as reduction in the expression of interferon-γ and other inflammatory cytokines in the mesenteric adipose tissue (MAT) of Lepr(db) mice. Furthermore, surgery improved endothelium-dependent, but not endothelium-independent, vasorelaxation in small mesenteric arteries (SMA) of Lepr(db) mice. The improvement in endothelial function was largely attenuated by nitric oxide synthase inhibitor (L-NAME) incubation. Interferon-γ treatment increased the mRNA expression of tumor necrosis factor-α in the MAT of control mice and incubation of SMA of control mice with tumor necrosis factor-α caused impairment of endothelial function. Superoxide production in MAT/SMA and nitrotyrosine protein level in SMA were elevated in diabetic mice. Surgery reduced MAT/SMA oxidative stress in Lepr(db) mice.
  
  
  CONCLUSIONS
  The amelioration of adipose tissue inflammation and the improvement of endothelial function may represent important mechanisms that result in cardiovascular benefits after bariatric surgery.
authors.affiliation: Department of Internal Medicine, Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA.
authors.forename: Hanrui
authors.initials: H
authors.lastname: Zhang
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Barry J
authors.initials: BJ
authors.lastname: Potter
authors.forename: James R
authors.initials: JR
authors.lastname: Sowers
authors.forename: Cuihua
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D050110:Bariatric Surgery; D017252:CD3 Complex / Q000235:genetics; D018932:Chemokine CCL2 / Q000235:genetics; D016207:Cytokines / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D007249:Inflammation / Q000517:prevention & control*; D050152:Intra-Abdominal Fat / Q000276:immunology / Q000473:pathology*; D008264:Macrophages / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D015431:Weight Loss
chemical_list: D017252:CD3 Complex; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016207:Cytokines; D009569:Nitric Oxide