A low‐saturated‐fat, low‐cholesterol diet decreases plasma CETP activity and pre β‐HDL formation but does not affect cellular cholesterol efflux to plasma from type 1 diabetic patients

Abstract

The aim of this study was to evaluate the effect of a low‐saturated‐fat, low‐cholesterol diet on plasma lipopoproteins, pre β‐high density lipoprotein (HDL) formation, lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) activities, as well as on the ability of plasma to stimulate cellular cholesterol efflux. Twelve male type 1 diabetic patients with plasma cholesterol >5.0 mmol/L were studied while consuming their usual diet and after 6 weeks of a low‐fat, low‐cholesterol diet. Pre β‐HDL formation was measured using crossed immuno‐electrophoresis. Plasma LCAT, CETP and PLTP activities were assayed by exogenous substrate methods. The ability of plasma to promote cellular cholesterol efflux out of Fu5AH rat hepatoma cells and out of human skin fibroblasts was also determined. Saturated fat intake was lowered (p = 0.001) due to replacement with carbohydrates, while mono‐ and polyunsaturated fat intake remained unchanged. Cholesterol intake decreased as well (p = 0.003). The changes in plasma total cholesterol, very low and low‐density lipoprotein (VLDL+LDL) cholesterol, HDL cholesterol, HDL phospholipids, apolipoprotein (apo) A‐I, plasma LCAT activity and PLTP activity were not significant. Plasma CETP activity (p = 0.008) and pre β‐HDL formation (p = 0.008) decreased. The ability of plasma to promote cholesterol efflux out of fibroblasts and Fu5AH cells remained unchanged. Reduction in dietary saturated fat and cholesterol intake does not adversely affect cellular cholesterol efflux to plasma from type 1 diabetic patients, despite a drop in pre β‐HDL formation.

• Cellular cholesterol efflux
• diet intervention
• high‐density lipoproteins
• lipid transfer proteins
• type 1 diabetes melllitus

Acknowledgements

The technical assistance of Dr. E. Blaauwwiekel, H. Elias, F. Sadeghi Niaraki, T. van Gent and L. M. Scheek is appreciated. Dr. R. de Vries is supported by a grant from the Dutch Diabetes Research Foundation (grant no. 2001.00.012).