Decreased Plasma Lipoprotein Lipase in Hypoadiponectinemia

An association independent of systemic inflammation and insulin resistance

  1. Maximilian von Eynatten, MD1,
  2. Jochen G. Schneider, MD1,
  3. Per M. Humpert, MD1,
  4. Gottfried Rudofsky, MD1,
  5. Nikolaus Schmidt, MD1,
  6. Patrizia Barosch, MD1,
  7. Andreas Hamann, MD1,
  8. Michael Morcos, MD1,
  9. Joerg Kreuzer, MD2,
  10. Angelika Bierhaus, PHD1,
  11. Peter P. Nawroth, MD1 and
  12. Klaus A. Dugi, MD1
  1. 1Department of Medicine I (Endocrinolgy and Metabolism), Ruprecht-Karls-University of Heidelberg, Heidelberg, Germany
  2. 2Department of Medicine III (Cardiology), Ruprecht-Karls-University of Heidelberg, Heidelberg, Germany
  1. Address correspondence and reprint requests to Maximilian von Eynatten, Department of Medicine I (Endocrinology and Metabolism), University of Heidelberg, INF 410, D-69120 Heidelberg, Germany. E-mail: maximilian.eynatten{at}med.uni-heidelberg.de

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.

RESEARCH DESIGN AND 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.

Footnotes

  • A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    • Accepted September 8, 2004.
    • Received July 9, 2004.
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