|Tilly-Kiesi, Marju - UNIV HELSINKI|
|Lichtenstein, Alice - HNRCA-TUFTS|
|Rintarahko, Jouko - UNIV HELSINKI|
|Taskinen, Marja-Ritta - UNIV HELSINKI|
Submitted to: Arteriosclerosis Thrombosis and Vascular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 15, 1997
Publication Date: N/A
Interpretive Summary: One of the risk factors for coronary artery disease is low blood levels of the fat particle high density lipoprotein (HDL) cholesterol. It is believed that the level of HDL cholesterol may be connected to an effect it may have on the blood levels of another fat, triglyceride, which increase in response to eating high fat foods. Individuals with a specific change, or mutation, in one type of protein, apolipoprotein A-I, have lower levels of HDL cholesterol. They also have lower levels of apolipoproteins A-I and A-II, and of Lp(AI:AII) HDL cholesterol. In this study, people with an apolipoprotein A-I mutation were compared with family members who did not have the mutation. This study looked at the levels of various particles in the blood after eating high fat meals to see what differences occurred in those with the mutation. It was observed that patients with the mutation did not have increases in triglyceride after eating the high fat meal, nor did they have increases in the Lp(AI:AII) HDL concentration. This study provides further insight into the ways in which the body responds to fat intake by showing that patients who do not accumulate triglycerides after fat intake do not have a corresponding increase in Lp(AI:AII). Through a better understanding of this mechanism, new methods to eliminate this risk factor may follow.
Technical Abstract: Subjects with apoA-I(Lys107->O) deletion mutation have reduced levels of plasma HDL cholesterol, apoA-I, apoA-II and Lp(AI:AII). In the present study, we describe the postprandial responses of apoA-I (Lys107->O) 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. 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. In both patients and control subjects, the plasma HDL2 mass increased in response to the fat meal, whereas HDL3 mass decreased. In control subjects, the triglyceride levels increased in both HDL2 and to a lesser extent in HDL3. 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. 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%. The Lp(AI:AII) concentration in HDL3 decreased in both groups, but the changes were nonsignificant. Our findings show that in postprandial state no accumulation of triglycerides in HDL subclasses occurs in patients with apoA-I (Lys107->O) and that these patients appear to lack the ability to respond to fat feeding by increasing the Lp(AI:AII) concentration in HDL2.