Role of plasma adiponectin on the HDL-cholesterol raising effect of atorvastatin in patients with type 2 diabetes^*

ABSTRACT

Objective: Adiponectin, secreted by adipose tissue, plays an important role in lipoprotein metabolism and also affects carbohydrate and insulin pathways. We studied the effects of atorvastatin treatment on plasma adiponectin and high density cholesterol (HDL) levels in patients with type 2 diabetes.

Research design and methods: In the ‘Diabetes Atorvastatin Lipid Intervention’ (DALI) study, a randomized placebo-controlled study on the effects of atorvastatin treatment in 194 patients with type 2 diabetes and mildly elevated plasma triglycerides, adiponectin levels, lipoproteins, cholesteryl ester transfer protein (CETP) mass, as well as postheparin lipoprotein lipase (LPL) and hepatic lipase (HL) activities were assessed at baseline and after 6 months of treatment (placebo, 10 mg or 80 mg atorvastatin).

Results: At baseline, plasma adiponectin levels were positively associated with HDL cholesterol (r = 0.40, p < 0.001), and apoA-I (r = 0.38, p < 0.001) in both males and females. Adiponectin was negatively associated with triglycerides (r = −0.26, p < 0.001) in males as well as in females. Atorvastatin treatment had no effect on plasma adiponectin levels. However, adiponectin levels at baseline significantly predicted the effect of atorvastatin treatment on HDL-cholesterol (p = 0.007), i.e. patients with the highest baseline plasma adiponectin concentration (tertile 3) displayed the largest increase in plasma HDL cholesterol during treatment (8–10%), while the HDL-cholesterol increase in tertile 1 was almost negligible (1–3%).

Conclusion: In this study, high baseline plasma adiponectin levels significantly affect the HDL-cholesterol response to atorvastatin treatment in patients with type 2 diabetes and therefore may play a role in defining future treatment strategy.

Key words: :

• Adiponectin
• Apolipoprotein A-I
• Atorvastatin
• Diabetes type 2
• HDL

Acknowledgements

Declaration of interest: The original DALI study was an investigator-driven study partly supported by an unrestricted grant from Parke-Davis, the Netherlands, which is now Pfizer, the Netherlands. J. J. P. Kastelein and E. J. Sijbrands have been involved in trials for various pharmaceutical companies, and have given lectures on behalf of various companies. G. M. Dallinga-Thie, A. van Tol and L. van der Zee do not have any competing interests to declare with respect to the contents of this article.

The authors thank all the contributors (patients, technicians and data managers) to the DALI study, and also thank Robin P. F. Dullaart for critical reading of the manuscript.

The original DALI study group (in alphabetical order): Erasmus Medical Center Rotterdam, Department of Internal Medicine (I. Berk-Planken, N. Hoogerbrugge, H. Jansen); Erasmus University Rotterdam, Departments of Biochemistry and Clinical Chemistry (H. Jansen); Gaubius Laboratory TNO-KvL, Leiden (H. M. G. Princen); Leiden University Medical Center (M. V. Huisman, M. A. van de Ree); University Medical Center Utrecht, Julius Center for General Practice and Patient Oriented Research (R. P. Stolk, F. V. van Venrooij); University Medical Center Utrecht, Division of Internal Medicine (J. D. Banga, G. M. Dallinga-Thie, F. V. van Venrooij).

Notes

* Results of this study have been previously presented at the ‘Drugs affecting Lipid Metabolism’ (DALM) meeting, New York (USA), October 2007