title: The role of adiponectin as a compensatory mediator for the primary secretory defect in latent autoimmune diabetes in adults.
abstract: BACKGROUND
  Increased adiposity in patients with newly diagnosed type 2 diabetes mellitus (DM), as well as in patients who do not have DM, affects the regulation of insulin sensitivity and the metabolic effects of adiponectin.
  
  
  OBJECTIVE
  The goal of this study was to investigate the relationship between plasma adiponectin levels and obesity in patients developing DM mainly due to an early decline in β-cell function.
  
  
  METHODS
  We studied 29 patients with latent autoimmune diabetes in adults (LADA), 38 patients with type 1 DM, and 55 healthy volunteers.
  
  
  RESULTS
  Plasma adiponectin levels, adjusted for body mass index (BMI), were higher in patients with type 1 DM than in controls (P < 0.001) and similar to those in patients with LADA (P = 0.464). Plasma adiponectin levels were higher in LADA patients compared with controls (P < 0.001). In LADA patients, plasma adiponectin levels, adjusted for BMI, correlated significantly with insulin resistance (β coefficient, -6.453 [2.772]; P = 0.028). Interestingly, this relationship in LADA patients was significant in more overweight patients (β coefficient, -7.142 [3.249]; P = 0.048) but not in leaner patients (P = 0.571), a finding that was not confirmed through the results in the controls (P = 0.520 and P = 0.992, respectively).
  
  
  CONCLUSIONS
  In patients with LADA, increases in plasma adiponectin levels, after adjustment for BMI, could act as a mediator for improvement in insulin sensitivity and thus compensate for the primary secretory defect. This effect seems more profound in more overweight subjects than in leaner subjects.
authors.affiliation: 2nd Department of Internal Medicine, Research Institute and Diabetes Center, Athens University, Attikon, University General Hospital, Athens, Greece. erihat@otenet.gr
authors.forename: Erifili
authors.initials: E
authors.lastname: Hatziagelaki
authors.forename: Vaia
authors.initials: V
authors.lastname: Lambadiari
authors.forename: Anastasia
authors.initials: A
authors.lastname: Tsiavou
authors.forename: Helen
authors.initials: H
authors.lastname: Gogas
authors.forename: Reinhard G
authors.initials: RG
authors.lastname: Bretzel
authors.forename: George
authors.initials: G
authors.lastname: Dimitriadis
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000378:metabolism; D000328:Adult; D015992:Body Mass Index; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000276:immunology; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood* / Q000503:physiopathology; D050177:Overweight; D012044:Regression Analysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; D007328:Insulin; D015850:Interleukin-6; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha
keywords: LADA; adiponectin; insulin sensitivity; type 1 diabetes mellitus