Surface binding, internalization and degradation by cultured human fibroblasts of low density lipoproteins isolated from type 1 (insulin-dependent) diabetic patients: changes with metabolic control.

Abstract:

:A previous study of low density lipoprotein metabolism by cultured cells focused on the metabolism of normal lipoproteins in vitro by fibroblasts isolated from diabetic patients. No abnormalities were found. We have followed the opposite approach. Using normal human fibroblasts as test cells we compared the metabolism in vitro of low density lipoproteins isolated from diabetic patients before and after metabolic control. We found a significant decrease (p less than 0.02) in internalization and degradation of low density lipoproteins isolated from diabetic patients before metabolic control when compared with those isolated from normal control subjects or from the same patients after metabolic control. The observed changes were mainly apparent in intracellular degradation. To evaluate whether the observed differences in low density lipoprotein behaviour were correlated with lipid or apolipoprotein composition, we measured cholesterol, triglyceride, apolipoprotein B and total protein levels in the low density lipoproteins tested. A significant decrease (p less than 0.05) of the triglyceride/protein ratio was found in post-control low density lipoproteins suggesting that a high triglyceride content may interfere with low density lipoprotein metabolism. The present study represents the first observation that metabolic control in diabetes mellitus can alter low density lipoprotein-cell interaction and suggests a possible mechanism for the enhanced incidence of atherosclerosis in diabetic patients.

journal_name

Diabetologia

journal_title

Diabetologia

authors

Lopes-Virella MF,Sherer GK,Lees AM,Wohltmann H,Mayfield R,Sagel J,LeRoy EC,Colwell JA

doi

10.1007/BF00282585

subject

Has Abstract

pub_date

1982-06-01 00:00:00

pages

430-6

issue

6

eissn

0012-186X

issn

1432-0428

journal_volume

22

pub_type

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