Exp Clin Endocrinol Diabetes 2001; Vol. 109(4): 548-559
DOI: 10.1055/s-2001-15117
Symposium Proceeding

© Johann Ambrosius Barth

Treatment of dyslipoproteinemia in the metabolic syndrome

A. Steinmetz1 , S. Fenselau2 , J. Schrezenmeir2
  • 1 St. Nikolaus-Stiftshospital, Teaching Hospital, University of Bonn at Andernach, Germany
  • 2 Institute for Physiology and Biochemistry Federal Research Centre, Kiel, Germany
Further Information

Publication History

Publication Date:
31 December 2001 (online)

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Summary:

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk to develop cardiovascular disease. The metabolic syndrome is characterized by atherogenic dyslipidemia (elevated triglycerides, increased small dense low-density lipoproteins, and decreased high-density lipoproteins), hypertension, insulin resistance and obesity. To decrease the risk of cardiovascular disease events decreasing body weight by ingesting a healthy diet, increasing physical activity, cessation of smoking and managing dyslipidemia are recommended. Pharmacological treatment of dyslipidemia is based on different drug classes. For LDL-cholesterol-lowering mainly statins and for triglyceride-lowering mainly fibrates are used. In primary and secondary prevention trials of heart disease they have shown to reduce the incidence of coronary artery disease or coronary events by 25-60 percent. Statins reduce mainly LDL-cholesterol levels by competitive inhibition of HMG-CoA reductase but have also shown to reduce fasting and postprandial triglyceride levels. Fibrates effectively reduce fasting and postprandial lipemia, shift the distribution of LDL particles towards less dense particles and increase HDL-cholesterol. Thus fibrates particularly address components of the metabolic syndrome and features of diabetic dyslipidemia. However studies still are needed showing definite evidence on differential therapy in lipid lowering based on prospective controlled trials with endpoints of macro- and microangiopathy in diabetic patients.

Abbreviations: BMI body mass index; CHD coronary heart disease; FFA free fatty acids; HDL high-density lipoprotein; HMG-CoA 3-hydroxy-3-methylglutaryl coenzyme A; IDL intermediate-density lipoprotein; LDL low-density lipoprotein; LPL lipoprotein lipase; NIDDM non-insulin-dependent diabetes mellitus; NO nitric oxide; PAI-1 plasminogen activator inhibitor-1; TRL triglyceride-rich lipoprotein; TG triglyceride; VLDL very-low-density lipoprotein

References

Prof. Dr. med. A. Steinmetz

St. Nikolaus-Stiftshospital GmbH Andernach

Teaching Hospital University of Bonn

Hindenburgwall 1

D-56626 Andernach, Germany

Phone: + 49-2632-404-5497/5498

Fax: + 49-2632-404-5640

Email: Armin.SteinmetzStiftshospital-Andernach