title: Association of impaired glucose metabolism in morbid obesity with hypoadiponectinaemia.
abstract: BACKGROUND
  Increased circulating levels of cytokines and chemokines and decreased adiponectin levels are associated with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). As obesity is the major risk factor for T2DM it is not clear why many patients with morbid obesity remain normoglycaemic and if this protection can be attributed to a lower grade of inflammation or higher adiponectin levels.
  
  
  METHODS
  Glucose tolerance of morbidly obese patients (n=2 754, body mass index > or =40 kg/m2) was assessed by oral glucose tolerance tests. In a case-control design we compared levels of eight immune mediators and adiponectin from patients with IGT/T2DM (n=52) and normal glucose tolerance (NGT; n=59). Gene expression in peripheral blood was determined by quantitative RT-PCR, and serum concentrations of immune mediators and adiponectin were measured by ELISA and bead-based multiplex technology.
  
  
  RESULTS
  About 54% of the patients in our morbidly obese cohort were normoglycaemic, while 14% were diagnosed with IGT and 32% with T2DM. There was no statistically significant difference in mRNA expression or serum levels of proinflammatory markers. Interestingly, we could demonstrate an association of NGT with higher adiponectin levels (p=0.039). Adiponectin levels were negatively correlated with interleukin (IL)-6 and macrophage chemoattractant protein (MCP)-1, but independent the other immune mediators.
  
  
  CONCLUSIONS
  We found an association of lower adiponectin levels with IGT/T2DM, but no further increase in inflammatory markers in morbid obesity. This suggests that in addition to chronic, low-grade inflammation, adiponectin is an important factor in the development of, or protection against, T2DM in obesity.
authors.affiliation: Department of Endocrinology, Diabetes and Rheumatology, University Hospital Düsseldorf, Germany. sven.schinner@uni-duesseldorf.de
authors.forename: S
authors.initials: S
authors.lastname: Schinner
authors.forename: K
authors.initials: K
authors.lastname: Kempf
authors.forename: H
authors.initials: H
authors.lastname: Overmann
authors.forename: H S
authors.initials: HS
authors.lastname: Willenberg
authors.forename: M
authors.initials: M
authors.lastname: Schott
authors.forename: B
authors.initials: B
authors.lastname: Rose
authors.forename: W A
authors.initials: WA
authors.lastname: Scherbaum
authors.forename: C
authors.initials: C
authors.lastname: Herder
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D000328:Adult; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D015331:Cohort Studies; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000235:genetics / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications* / Q000235:genetics / Q000276:immunology; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood / Q000150:complications* / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D052242:Adiponectin; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D012333:RNA, Messenger; D005947:Glucose