Postprandial responses of plasma lipids and lipoproteins in subjects with apoA-I(Lys107-->0).
Subjects with apoA-I(Lys107-->0) deletion mutation have reduced levels of plasma HDL cholesterol, apoA-I, apoA-II and Lp(AI:AII). In the present study were describe the postprandial responses of apoA-I(Lys107-->0) subjects (n=6) to the ingestion of a fat rich meal compared to the responses of their unaffected family members (n=6). The postprandial plasma triglyceride responses were comparable in the two groups of subjects. Plasma postprandial HDL cholesterol levels fell in both groups; patients (0.89+/-0.05-0.76+/-0.06 mmol/l, P=0.0032) and control subjects (1.32+/-0.25-1.18+/-0.21 mmol/l; P=0.0022). HDL2 cholesterol levels tended to rise, but the changes were not significant. By contrast, in both patients and control subjects, the HDL3 cholesterol levels fell; patients (0.52+/-0.15-0.37+/-0.11 mmol/l, P=0.0068) and control subjects (0.63+/-0.10-0.49+/-0.08 mmol/l, P=0.0078), respectively. In both patients and control subjects the plasma HDL2 mass increased in response to the fat meal; patients (94.7+/-37.3-114.3+/-28.8 mg/dl, P=0.0397) and control subjects (142.1+/-32.8-168.1+/-29.8 mg/dl, P=0.0298), whereas HDL3 mass decreased; patients (162.3+/-36.8-131.4+/-28.9 mg/dl, P=0.0251) and control subjects (185.5+/-34.1-161.1+/-29.0 mg/dl, P=0.0021), respectively. In control subjects the triglyceride levels increased in both HDL2 (0.10+/-0.06-0.17+/-0.06 mmol/l; P=0.0005) and to a lesser extent in HDL3 (0.10+/-0.03-0.12+/-0.02 mmol/l, P=0.0017). In patients, triglyceride levels in both HDL subclasses remained unchanged. Changes in the concentration of Lp(AI) in HDL2 and HDL3 were comparable in the two groups of subjects. The Lp(AI:AII) concentration in HDL2 remained unchanged in the patients, but increased in control subjects (change+27%. P=0.0026). Consequently, the 20% difference at baseline in the concentration of Lp(AI:AII) in HDL2 between the patients and control subjects increased postprandially to 45% (P=0.0240). The Lp(AI:AII) concentration in HDL3 decreased in both groups, but the changes were non-significant. Our findings show that in postprandial state, no accumulation of triglycerides in HDL subclasses occurs in patients with apoA-I(Lys[107]-->0) and that these patients appear to lack the ability to respond to fat feeding by increasing the Lp(AI:AII) concentration in HDL2.
Tilly-Kiesi
M
M
Department of Medicine, Helsinki University Central Hospital, Finland.
Lichtenstein
A H
AH
Rintarahko
J
J
Taskinen
M R
MR
D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood / Q000235:genetics*; D016633:Apolipoprotein A-II / Q000097:blood; D001053:Apolipoproteins / Q000097:blood; D016022:Case-Control Studies; D015243:Cholesterol, VLDL / Q000097:blood; D005260:Female; D017353:Gene Deletion; D006801:Humans; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008239:Lysine / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics / Q000502:physiology; D019518:Postprandial Period / Q000502:physiology*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001053:Apolipoproteins; D015243:Cholesterol, VLDL; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; D008239:Lysine