title: Decreased plasma lipoprotein lipase in hypoadiponectinemia: an association independent of systemic inflammation and insulin resistance.
abstract: OBJECTIVE
  Adiponectin is a plasma protein expressed in adipose tissue. Hypoadiponectinemia is associated with low HDL cholesterol and high plasma triglycerides, which also characterize lipoprotein lipase (LPL) deficiency syndromes. Recently, dramatically increased LPL activity was reported in mice overexpressing adiponectin. We therefore speculated that adiponectin may directly affect LPL in humans.
  
  
  METHODS
  We measured plasma adiponectin and postheparin LPL in 206 nondiabetic men and in a second group of 110 patients with type 2 diabetes. Parameters were correlated with markers of systemic inflammation (C-reactive protein [CRP]) and insulin resistance (homeostatis model assessment of insulin resistance [HOMA-IR]).
  
  
  RESULTS
  Nondiabetic subjects with decreased plasma adiponectin had lower LPL activity (r=0.42, P <0.0001). This association of plasma adiponectin with LPL activity was confirmed in the second group of patients with type 2 diabetes (r=0.37, P <0.0001). Multivariate analysis revealed that adiponectin was the strongest factor influencing LPL activity, accounting for 23% of the variation in LPL activity in nondiabetic subjects and for 26% of the variation in LPL activity in type 2 diabetic patients. These associations were independent of plasma CRP and HOMA-IR.
  
  
  CONCLUSIONS
  These results demonstrate an association of decreased postheparin LPL activity with low plasma adiponectin that is independent of systemic inflammation and insulin resistance. Therefore, LPL may represent a link between low adiponectin levels and dyslipidemia in both nondiabetic individuals and patients with type 2 diabetes.
authors.affiliation: Department of Medicine I (Endocrinology and Metabolism), University of Heidelberg, INF 410, D-69120 Heidelberg, Germany. maximilian.eynatten@med.uni-heidelberg.de
authors.forename: Maximilian
authors.initials: M
authors.lastname: von Eynatten
authors.forename: Jochen G
authors.initials: JG
authors.lastname: Schneider
authors.forename: Per M
authors.initials: PM
authors.lastname: Humpert
authors.forename: Gottfried
authors.initials: G
authors.lastname: Rudofsky
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Schmidt
authors.forename: Patrizia
authors.initials: P
authors.lastname: Barosch
authors.forename: Andreas
authors.initials: A
authors.lastname: Hamann
authors.forename: Michael
authors.initials: M
authors.lastname: Morcos
authors.forename: Joerg
authors.initials: J
authors.lastname: Kreuzer
authors.forename: Angelika
authors.initials: A
authors.lastname: Bierhaus
authors.forename: Peter P
authors.initials: PP
authors.lastname: Nawroth
authors.forename: Klaus A
authors.initials: KA
authors.lastname: Dugi
mesh_terms: D052242:Adiponectin; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood; D007249:Inflammation / Q000097:blood / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood* / Q000172:deficiency*; D008071:Lipoprotein Lipase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012016:Reference Values; D012044:Regression Analysis; D014280:Triglycerides / Q000097:blood
chemical_list: D052242:Adiponectin; D008076:Cholesterol, HDL; D036341:Intercellular Signaling Peptides and Proteins; D014280:Triglycerides; D008071:Lipoprotein Lipase