Abnormal metabolism of postprandial lipoproteins in patients with non-insulin-dependent diabetes mellitus is not related to coronary artery disease.
To investigate whether abnormalities in alimentary lipemia explain the increased risk of coronary artery disease (CAD) in subjects with non-insulin-dependent diabetes mellitus (NIDDM), we performed an oral vitamin A fat-load test in four groups of men (each n = 15): 1) NIDDM and angiographically verified CAD (DM+CAD+): 2) CAD but no diabetes (DM-CAD+); 3) NIDDM but no CAD, excluded by an exercise thallium scan (DM+CAD-); and 4) healthy control subjects (DM-CAD-). The groups were matched for age and body mass index. Plasma obtained after an overnight fast and 2, 3, 4, 6, 9, 12, and 24 h after a fatty meal (78 g fat, 345,000 IU retinyl palmitate [RP]) was separated by density gradient ultracentrifugation into six fractions of triglyceride (TG)-rich lipoproteins: Svedberg flotation units (Sf) > 3200, Sf 1100-3200, Sf 400-1100, Sf 60-400, Sf 20-60, and Sf 12-20. TG, RP, and cholesterol concentrations were measured in plasma and in each lipoprotein fraction. Postprandial plasma TG responses were significantly larger in both NIDDM groups than in the healthy control group. The most marked differences were observed in the Sf 60-400 lipoproteins, whether measured as TG or RP responses. However, there were no differences between the DM+CAD+ and DM+CAD- groups. The between-group differences in alimentary lipemia were only partially explained by fasting TG levels. In contrast to the healthy subjects, no significant negative correlation was observed in the NIDDM patients between alimentary lipemia and lipoprotein lipase activity, implying an abnormality of the lipolysis of TG-rich particles in NIDDM. Levels of atherogenic postprandial remnant lipoproteins are increased in NIDDM. However, in this study the magnitude of alimentary lipemia did not distinguish NIDDM patients with CAD from those without CAD symptoms and normal exercise thallium scans.
Syvänne
M
M
First Department of Medicine, University of Helsinki, Finland.
Hilden
H
H
Taskinen
M R
MR
D000368:Aged; D001057:Apolipoproteins E / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000150:complications* / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications*; D004041:Dietary Fats / Q000008:administration & dosage; D004224:Diterpenes; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000150:complications; D007328:Insulin / Q000097:blood; D008049:Lipase / Q000097:blood; D008071:Lipoprotein Lipase / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D053419:Lipoproteins, IDL; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D000084562:Retinyl Esters; D014280:Triglycerides / Q000097:blood; D014801:Vitamin A / Q000031:analogs & derivatives / Q000097:blood
D001057:Apolipoproteins E; D001786:Blood Glucose; D004041:Dietary Fats; D004224:Diterpenes; D007328:Insulin; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D053419:Lipoproteins, IDL; D008079:Lipoproteins, VLDL; D017395:Plasminogen Activator Inhibitor 1; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate; D002784:Cholesterol; D008049:Lipase; D008071:Lipoprotein Lipase