Postprandial responses of plasma lipids and lipoproteins in subjects with apoA-I(Lys107→0) Original Research Article

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 remaind 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(Lys107→0) and that these patients appear to lack the ability to respond to fat feeding by increasing the Lp(AI:AII) concentration in HDL2.