title: Oxidation of low-density lipoprotein in NIDDM: its relationship to fatty acid composition.
abstract: The increased risk of atherosclerotic disease in diabetic subjects may be due to enhanced foam cell formation following an increased susceptibility of low density lipoprotein to oxidative modification. This study has compared fatty acid content and lipoprotein oxidisability in 10 non-insulin-dependent diabetic subjects with that in 10 control subjects. Both groups were normocholesterolaemic and the diabetic subjects had higher triglyceride levels (2.2 +/- 0.4 vs 1.2 +/- 0.2 mmol/l, p < 0.05). The fatty acid composition was compared in low density lipoprotein following Folch extraction, separation by thin layer chromatography (for the lipid classes) and analysis by gas liquid chromatography. Low density lipoprotein oxidisability was assessed by conjugated diene and thiobarbituric acid reacting substance formation in the presence of copper ions. The esterified/free cholesterol ratio was higher in the low density lipoprotein from patients compared to control subjects (2.9 +/- 0.1 vs 1.9 +/- 0.3, p < 0.05). Linoleic acid in the cholesteryl ester fraction of the lipoprotein was higher in the patients than in the control subjects (48.2 +/- 2.2% vs 42.4 +/- 3.4%, p < 0.05) as was the total quantity of linoleic acid in the cholesteryl ester fraction (317.8 +/- 68.0 vs 213.2 +/- 28.0 micrograms/mg protein, p < 0.05) and in the low-density lipoprotein as a whole (443.2 +/- 70.0 vs 340.2 +/- 28.2 micrograms/mg protein, p < 0.05). Lipoprotein oxidisability was also increased in the diabetic group with increased formation of thiobarbituric acid reacting substances (35.6 +/- 7.2 vs 22.3 +/- 3.5 nmol/mg protein, p < 0.05, increased total diene formation (502 +/- 60 vs 400 +/- 30 nmol/mg protein, p < 0.05) and increased rate of diene formation (7.2 +/- 0.6 vs 5.1 +/- 0.9 nmol diene.mg protein-1.min-1, p < 0.05). This study indicates that low-density lipoprotein from diabetic subjects is more susceptible to oxidation. This could, in vivo, accelerate foam-cell formation thereby increasing atherosclerotic risk in diabetic subjects.
authors.affiliation: Department of Clinical Medicine, Trinity College, Dublin, Republic of Ireland.
authors.forename: E
authors.initials: E
authors.lastname: Dimitriadis
authors.forename: M
authors.initials: M
authors.lastname: Griffin
authors.forename: D
authors.initials: D
authors.lastname: Owens
authors.forename: A
authors.initials: A
authors.lastname: Johnson
authors.forename: P
authors.initials: P
authors.lastname: Collins
authors.forename: G H
authors.initials: GH
authors.lastname: Tomkin
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D014280:Triglycerides / Q000097:blood
chemical_list: D005227:Fatty Acids; D008077:Lipoproteins, LDL; D014280:Triglycerides