Pravastatin in diabetes-associated hypercholesterolemia

Abstract

Patients with diabetes mellitus (DM), type 1 and type 2, have an increased risk of coronary heart disease as a result of accelerated atherosclerosis. Dyslipidemia, often found in these patients, plays an important role in this process. This study investigates the efficacy and safety of lipid-lowering therapy with pravastatin, a 3-HMG-Coenzym A reductase inhibitor in hypercholesterolemic type-1 and type-2 diabetic patients. Of 49 patients (22 type-1 DM and 27 type-2 DM), 24 patients were treated with pravastatin, 20 mg/day, and 25 patients with placebo. After 24 weeks, total cholesterol (TC) was decreased by 22.2%, low-density lipoprotein (LDL) cholesterol by 25.8% and triglycerides (TG) by 13.6%. Pravastatin treatment did not induce a significant change in high-density (HDL) cholesterol levels. No differences in effects of pravastatin treatment on serum lipids and lipoproteins were found with respect to the diabetes type. No serious side effects occurred and pravastatin treatment did not cause any deterioration in glycemia control. The data suggest that pravastatin is effective and safe in the treatment of dyslipidemia in both type-1 and type-2 diabetic patients.

Statin therapy depresses total body fat oxidation in the absence of genetic limitations to fat oxidation

“…The ratios of LDL-C/HDL-C (19%) and TC/HDL-C (29%) decreased during statin therapy (Castano et al 1999). The benefits of statin therapy observed in blood lipoproteins are not associated with a deterioration in glycaemic control, while an inhibition of lipid peroxidation has been reported (Rustemeijer et al 1997). The reductions in lipoproteins reported have been attributed to suppression of their biosynthesis (Qureshi and Peterson 2001) and availability; however, their transport and use by the mitochondria may also be affected.…”

“…Although the responses are drug-and dosedependent, in general, both animal and human studies report a decrease in total cholesterol (TC) (14-30%), low-density-lipoprotein cholesterol (LDL-C) (16-42%), very-low-density-lipoprotein cholesterol (VLDL-C) (8%), apolipoprotein B (13-38%), triacylglycerol (11-23%), thromboxane B 2 (34%) and platelet factor 4 (26%) from 10-20 mg doses of statins (Castano et al 1999;Iliadis and Rosenson 1999;Rustemeijer et al 1997;Smith et al 2000;Zambon et al 1999). Most studies have failed to demonstrate increased high-density-lipoprotein cholesterol (HDL-C) or apolipoprotein A1 during statin therapy (Castano et al 1999;Rustemeijer et al 1997;Zambon et al 1999). The ratios of LDL-C/HDL-C (19%) and TC/HDL-C (29%) decreased during statin therapy (Castano et al 1999).…”

Membrane cholesterol modulates the fluid shear stress response of polymorphonuclear leukocytes via its effects on membrane fluidity

“…In general, chronic inflammation is a common denominator for a wide range of cardiovascular disease conditions including diabetes and hypercholesterolemia, both of which involve development of a hyperlipidemic blood environment (45). As such, the possibility that elevated blood cholesterol alters leukocyte sensitivity to fluid flow through its effects on the cell membrane implicates aberrant or dysfunctional leukocyte mechanotransduction in this pathological condition.…”

Cellular cholesterol efflux to plasma from moderately hypercholesterolaemic type 1 diabetic patients is enhanced, and is unaffected by simvastatin treatment

“…HMG (hydroxymethylglutaryl) Co-A reductase inhibitors are well known to reduce LDL cholesterol as well as plasma triglyceride levels [17,18], and to lower the incidence of cardiovascular disease [19][20][21]. Even with average cholesterol levels, statins have been proven to be beneficial [22], making it important to study the effects of statins in type 1 diabetes.…”