title: Association of adipokines and inflammatory markers with lipid control in type 2 diabetes.
abstract: BACKGROUND
  Data regarding the effect of certain adipokines on lipid metabolism are equivocal.
  
  
  OBJECTIVE
  The aim of this study was to evaluate the association of lipid control with adipokines and inflammatory markers in patients with type 2 diabetes.
  
  
  METHODS
  The analysis included 195 patients with type 2 diabetes. The achievement of treatment targets in terms of total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides was assessed in accordance with the current guidelines. Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) index as well as concentrations of highmolecular-weight (HMW) adiponectin, leptin, resistin, high-sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α (TNF-α) were measured in all patients. Logistic regression analyses were performed to determine the risk factors for inadequate lipid control.
  
  
  RESULTS
  Optimal control in terms of total cholesterol, LDL, HDL, and triglycerides was achieved in 61%, 43%, 53%, and 68% of the patients, respectively. In multivariate analyses, female sex, lower resistin concentrations, and the absence of statin treatment were predictors of total cholesterol levels above the treatment target; older age and lower statin dose--of LDL cholesterol levels above the treatment targets; female sex, higher HOMA-IR index, lower HMW adiponectin concentrations, and higher TNF-α concentration-o-f HDL levels below the treatment targets; and higher HOMA-IR, lower HMW adiponectin concentration, and the absence of statin treatment--of triglycerides above the treatment target.
  
  
  CONCLUSIONS
  In type 2 diabetes, lower HMW adiponectin concentrations are associated with inadequate triglyceride and HDL control; higher TNF-α, with inadequate HDL control, and lower resistin concentrations, with inadequate total cholesterol control.
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Kapłon-Cieślicka
authors.forename: Marek
authors.initials: M
authors.lastname: Postuła
authors.forename: Marek
authors.initials: M
authors.lastname: Rosiak
authors.forename: Michał
authors.initials: M
authors.lastname: Peller
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Kondracka
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Serafin
authors.forename: Ewa
authors.initials: E
authors.lastname: Trzepla
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Opolski
authors.forename: Krzysztof J
authors.initials: KJ
authors.lastname: Filipiak
mesh_terms: D054392:Adipokines / Q000097:blood*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation; D050356:Lipid Metabolism; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D054392:Adipokines; D015415:Biomarkers; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D002784:Cholesterol