Metabolic heterogeneity underlying postprandial lipemia among men with low fasting high density lipoprotein cholesterol concentrations.
The high triglyceride (TG) and low high density lipoprotein (HDL) cholesterol dyslipidemia has been associated with increased postprandial lipemia. Although fasting TG is a powerful predictor of postprandial hyperlipidemia, the role of hypoalphalipoproteinemia in postprandial TG metabolism is uncertain. We have studied postprandial lipemia among 63 men with low fasting plasma HDL cholesterol concentrations (<0.9 mmol/L), but with either low (<2.0 mmol/L) or high (>2.0 mmol/L) fasting plasma TG levels. A significant relationship was noted between postprandial TG response and fasting HDL cholesterol concentration (r = -0.43; P: < 0.0005). We also found that men with high TG/low HDL dyslipidemia (high TG and low HDL cholesterol; n = 16) were characterized by abdominal obesity as well as increased visceral adipose tissue accumulation, whereas normolipidemic controls (low TG and high HDL cholesterol; n = 26) and men with isolated low HDL cholesterol concentrations (low TG and low HDL cholesterol; n = 17) were not characterized by features of the insulin resistance syndrome (visceral obesity, hyperinsulinemia, and hypertriglyceridemia). Although controls and men with isolated low HDL cholesterol levels had similar postprandial lipemic responses, men with the high TG/low HDL dyslipidemia had a marked increase in their postprandial TG responses to the fat load compared with the other subgroups (P: < 0. 001). Men with the high TG/low HDL dyslipidemia were also characterized by higher concentrations of apolipoprotein (apo) B-48 and B-100 particles (chylomicron remnants and very low density lipoproteins, respectively) before and during the postprandial period compared with the other subjects. These results suggest that low HDL cholesterol concentration is a heterogeneous metabolic phenotype that it is not associated with postprandial hyperlipidemia unless accompanied by other features of the insulin resistance syndrome.
Couillard
C
C
Lipid Research Center, Laval University Medical Research Center, CHUL Pavilion, Sainte-Foy, Québec, Canada G1V 4G2.
Bergeron
N
N
Bergeron
J
J
Pascot
A
A
Mauriège
P
P
Tremblay
A
A
Prud'homme
D
D
Bouchard
C
C
Després
J P
JP
D000273:Adipose Tissue / Q000502:physiology; D000328:Adult; D053299:Apolipoprotein B-100; D053283:Apolipoprotein B-48; D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D001835:Body Weight; D008076:Cholesterol, HDL / Q000097:blood / Q000235:genetics*; D005215:Fasting / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood / Q000235:genetics*; D008071:Lipoprotein Lipase / Q000097:blood; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period / Q000235:genetics*; D014280:Triglycerides / Q000097:blood
D053299:Apolipoprotein B-100; D053283:Apolipoprotein B-48; D001055:Apolipoproteins B; D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D008055:Lipids; D014280:Triglycerides; D008071:Lipoprotein Lipase