Comparison of antioxidant activity in lipoprotein fractions from insulin-dependent diabetics and healthy controls.
The insulin-dependent diabetic patient is at greatly increased risk of premature atherosclerosis. Oxidative damage to lipoproteins has been implicated as an important factor in the atherogenic process. Diabetic patients are exposed to excessive oxidative stress because of non-enzymatic glycation of proteins and a variety of defects in antioxidant systems. We have previously described an enhanced chemiluminescent method for measuring protective 'chain-breaking' antioxidant activity in plasma lipoprotein fractions. In this study we compare the lipid content and antioxidant activity of plasma lipoproteins in 22 young insulin-dependent diabetics without vascular complications and 20 age- and sex-matched controls. Mean levels of haemoglobin A 1c in the diabetic group were 8.8 +/- 0.2%. There were no significant differences in serum total cholesterol, apolipoprotein A, apolipoprotein B or lipoprotein(a) levels between the study groups. Serum total triglyceride levels (1.32 +/- 0.11 versus 1.01 +/- 0.08 mmol/l; P < 0.05) and LDL-associated triglyceride (0.28 +/- 0.04 versus 0.15 +/- 0.02 mmol/l; P < 0.05) were significantly elevated in the diabetic group. Total plasma antioxidant activity was significantly reduced in the diabetic group (272.0 +/- 15.4 versus 338.3 +/- 20.7 micromol/l; P < 0.05). Antioxidant activity measured in five lipoprotein fractions isolated by density gradient ultracentrifugation (VLDL1. VLDL2, LDL1, LDL2 and HDL) showed no significant differences between groups when corrected for protein, total lipid or cholesterol content. When corrected for triglyceride content significantly lower antioxidant values were found in the diabetic HDL fraction only. The results of this study imply that the susceptibility of the insulin-dependent diabetic to the development of premature atherosclerosis cannot be attributed to reduced antioxidant activity in circulating plasma lipoproteins.
Maxwell
S
S
Wallenberg Laboratory for Cardiovascular Research, Sahlgren's Hospital, Gothenberg, Sweden.
Holm
G
G
Bondjers
G
G
Wiklund
O
O
D000328:Adult; D000975:Antioxidants / Q000378:metabolism*; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology; D002784:Cholesterol / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006031:Glycosylation; D006801:Humans; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008163:Luminescent Measurements; D008297:Male; D018384:Oxidative Stress / Q000502:physiology; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014461:Ultracentrifugation
D000975:Antioxidants; D002784:Cholesterol; D006442:Glycated Hemoglobin; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D014280:Triglycerides; C032607:low density lipoprotein triglyceride