Modulation of low density lipoprotein subclasses by alimentary lipemia in control and normotriglyceridemic non-insulin-dependent diabetic subjects

Conventional factors do not fully account for the increased cardiovascular risk in NIDDM but, because of the underlying disorders in lipid metabolism, the postprandial state can be expected to induce temporary changes of a potentially atherogenic nature. The response to a 1000-kcal meal (70% lipid;...

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Veröffentlicht in:Atherosclerosis 1995-03, Vol.113 (2), p.197-209
Hauptverfasser: Attia, Nebil, Durlach, Vincent, Paul, Jean-Louis, Soni, Theophile, Betoulle, Dina, Girard-Globa, Anik
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Sprache:eng
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Zusammenfassung:Conventional factors do not fully account for the increased cardiovascular risk in NIDDM but, because of the underlying disorders in lipid metabolism, the postprandial state can be expected to induce temporary changes of a potentially atherogenic nature. The response to a 1000-kcal meal (70% lipid; 100 000 IU vitamin A) over 8 h was compared in 10 normoponderal, normotriglyceridemic NIDDM male patients and 12 controls. In patients lipolysis was normal, but remnant clearance was delayed ( P < 0.02) and apo E concentrations were lower. LDL-C decreased postprandially, more in patients ( P < 0.05), while LDL-PL accumulated in controls but not in patients. As a result UC:PL decreased in controls ( P < 0.05) not in patients. The distribution of LDL subclasses shifted towards large particles in controls (LDL-I, 42%; LDL-II, 50%; LDL-III, 7.6% at 6 h) and smaller ones in patients (LDL-I, 29%; LDL-II, 56%; LDL-III, 16% at 6 h). In controls only, the percentage of LDL-III correlated negatively with apo E ( r = − 0.97, P < 0.001) suggesting that apo E promotes removal of light particles before they reach LDL-III and may be a limiting factor in patients. We conclude that the postprandial state is potentially more atherogenic in normoponderal, normotriglyceridemic patients than in controls: remnant clearance is delayed, the UC:PL ratio of LDL fails to decrease postprandially as it does in controls, limiting the acceptor capacity of LDL for UC, and the distribution of LDL subclasses is shifted towards a more atherogenic profile.
ISSN:0021-9150
1879-1484
DOI:10.1016/0021-9150(94)05447-Q