title: Visceral fat resection in humans: effect on insulin sensitivity, beta-cell function, adipokines, and inflammatory markers.
abstract: OBJECTIVE
  The visceral fat is linked to insulin resistance, the metabolic syndrome, type 2 diabetes and an increased cardiovascular risk, but it is not clear whether it has a causative role.
  
  
  METHODS
  Surgical resection of this fat depot is a research model to address this issue. Twenty premenopausal women with metabolic syndrome and grade III obesity were randomized to undergo Roux-en-Y gastric bypass (RYGBP) either alone or combined with omentectomy. Insulin sensitivity (IS; euglycemic-hyperinsulinemic clamp), acute insulin response to glucose (AIR; intravenous glucose tolerance test), disposition index (DI = AIR × IS measured by clamp), lipid profile, adipokine profile (leptin, adiponectin, resistin, visfatin, interleukin-6, TNF-α, MCP-1), ultra-sensitive C-reactive protein (CRP), body composition, and abdominal fat echography were assessed prior to surgery and 1, 6, and 12 months post-surgery.
  
  
  RESULTS
  Omentectomy was associated with greater weight loss at all time points. IS improved similarly in both groups. Omentectomy was associated to lower CRP after 12 months, but it did not influence adipokines and other metabolic parameters. Among non-diabetic subjects, omentectomy was associated with a preservation of baseline AIR after 12 months (as opposed to deterioration in the control group) and a greater DI after 6 and 12 months.
  
  
  CONCLUSIONS
  Although omentectomy did not enhance the effect of RYGBP on insulin sensitivity and adipokines, it was associated with a preservation of insulin secretion, a greater weight loss, and lower CRP.
authors: Laboratory of Investigation in Metabolism and Diabetes (LIMED)/Gastrocentro, State University of Campinas (UNICAMP), Campinas, São Paulo, Brazil. endo.marcelolima@gmail.com
authors: Marcelo M O
authors: MM
authors: Lima
authors: Jose C
authors: JC
authors: Pareja
authors: Sarah M
authors: SM
authors: Alegre
authors: Sylka R
authors: SR
authors: Geloneze
authors: Steven E
authors: SE
authors: Kahn
authors: Brenno D
authors: BD
authors: Astiarraga
authors: Élinton A
authors: ÉA
authors: Chaim
authors: Jamal
authors: J
authors: Baracat
authors: Bruno
authors: B
authors: Geloneze
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose; D001823:Body Composition; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000503:physiopathology / Q000517:prevention & control; D018932:Chemokine CCL2 / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology / Q000517:prevention & control; D005260:Female; D015390:Gastric Bypass; D005951:Glucose Tolerance Test; D006801:Humans; D007249:Inflammation / Q000503:physiopathology / Q000517:prevention & control; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000503:physiopathology / Q000601:surgery*; D020738:Leptin / Q000097:blood; D024821:Metabolic Syndrome / Q000503:physiopathology / Q000601:surgery; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood; D009765:Obesity / Q000503:physiopathology / Q000601:surgery; D017697:Premenopause; D011446:Prospective Studies; D052243:Resistin / Q000097:blood; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015431:Weight Loss; D055815:Young Adult
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D015850:Interleukin-6; D020738:Leptin; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase