title: Comparison of metabolic effects of surgical-induced massive weight loss in patients with long-term remission versus non-remission of type 2 diabetes.
abstract: BACKGROUND
  The aim of this study was to evaluate the pathophysiological mechanisms underlying the non-remission of type 2 diabetes in Roux-en-Y gastric bypass (RYGB) patients.
  
  
  METHODS
  A group of patients not in remission (NR) was formed (n = 13). A remission group (R) was composed of patients who had undergone normalization of fasting glycemia and A1c, without anti-diabetic drugs and matched for selected baseline characteristics (i.e., duration of disease, previous BMI, final BMI, fat distribution, and age; n = 15). A control group of lean subjects (n = 41) was formed.
  
  
  RESULTS
  The NR group had higher uric acid (5.1 vs. 3.9 mg/dL), number of leukocytes (6,866.9 vs. 5,423.6), hs-CRP (0.27 vs. 0.12 mg/dL), MCP-1 (118.4 vs. 64.4 ng/mL), HOMA-IR, and AUC(glucose) but lower adiponectin (9.4 vs. 15.4 ng/mL), leptin (12.7 vs. 20.7 ng/mL), and AUC(GLP-1) in comparison to R group; the NR group also had lower leptin and higher adiponectin, HOMA-IR, AUC(glucose), AUC(C-peptide), AUC(glucagon), and AUC(GLP-1) than controls. The R group had lower MCP-1 and higher adiponectin compared to controls. Insulin sensitivity was significantly lower in the NR group than in the R and control groups. The insulin secretion index values were lower in the NR group than in the R and control groups.
  
  
  CONCLUSIONS
  This study found greater insulin resistance, lower insulin secretion, persistent adiposopathy and chronic subclinical inflammation, and less robust incretin response in the NR group despite a similar level of weight loss. Persistently altered pathophysiological mechanisms can be related to the lack of remission of type 2 diabetes after RYGB.
authors.affiliation: LIMED, Laboratory of Investigation on Metabolism and Diabetes, State University of Campinas, UNICAMP, Rua Carlos Chagas 420, 13082-970, Campinas, Brazil. fernandafilgueira@hotmail.com
authors.forename: Fernanda Filgueira
authors.initials: FF
authors.lastname: Hirsch
authors.forename: Jose Carlos
authors.initials: JC
authors.lastname: Pareja
authors.forename: Sylka Rodovalho
authors.initials: SR
authors.lastname: Geloneze
authors.forename: Elinton
authors.initials: E
authors.lastname: Chaim
authors.forename: Everton
authors.initials: E
authors.lastname: Cazzo
authors.forename: Bruno
authors.initials: B
authors.lastname: Geloneze
mesh_terms: D052242:Adiponectin / Q000097:blood; D000293:Adolescent; D000328:Adult; D019540:Area Under Curve; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D001938:Brazil / Q000453:epidemiology; D002097:C-Reactive Protein / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology / Q000601:surgery; D005260:Female; D015390:Gastric Bypass / Q000379:methods*; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006801:Humans; D054795:Incretins / Q000097:blood; D007962:Leukocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood* / Q000453:epidemiology / Q000601:surgery*; D012074:Remission Induction; D012189:Retrospective Studies; D014527:Uric Acid / Q000097:blood; D015431:Weight Loss; D055815:Young Adult
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D054795:Incretins; D014527:Uric Acid; D052216:Glucagon-Like Peptide 1; D002097:C-Reactive Protein