Influence of apo E phenotype on postprandial triglyceride and glucose responses in subjects with and without coronary heart disease

Apolipoprotein E phenotypes and fasting lipid and other biochemical parameters were determined in 51 patients with recently diagnosed coronary heart disease (CHD) and 164 control subjects. The age of the participants was 62.5±6.6 (S.D.) and 63% were male. Forty-eight CHD cases and 51 control subjects were also studied for 8 h after a fat-rich meal. Apo E phenotypes did not differ significantly between CHD cases and control subjects although there was a tendency for under-representation of E2/E3 in the cases (6% versus 16%). Fifteen CHD cases and 37 (of 164) control subjects had at least one 4 allele. Fasting plasma triglyceride concentrations were not different between CHD cases and controls but were significantly elevated in subjects with an 4 allele. CHD cases did, however, have a significantly elevated fasting insulin compared with controls. Postprandial triglyceride responses were not different between CHD cases and controls. However, postprandial triglyceride responses were elevated in subjects (CHD cases and controls) who had an 4 allele. In multivariate analysis, both 4 allele status and body mass index (BMI) were significant determinants of postprandial triglyceride responses. Postprandial glucose responses were also elevated in subjects with an 4 allele. When comparison of CHD cases and controls was restricted to those without an 4 allele, CHD cases showed a borderline significant (P=0.05) difference in time course from controls, with a slower decline in plasma triglyceride from the peak response. Fasting and postprandial triglyceride and postprandial glucose responses are strongly dependent on the presence of an 4 allele. The elevation in postprandial triglyceride responses associated with an 4 allele can obscure differences associated with the presence of CHD and suggests that although elevated postprandial triglyceride response may be a risk factor for CHD, it is not the major reason for the association between the possession of an 4 allele and coronary disease.