Moderate increase in dietary sucrose does not influence fasting or postprandial serum lipids regardless of the presence of apolipoprotein E2 allele in healthy subjects

Abstract

Objective: To investigate whether a moderate increase in dietary sucrose intake induces different serum lipid responses in normolipidemic subjects with the e2 allele compared with subjects without the e2 allele. Design: Controlled, parallel study. Subjects: There were 15 subjects with the apolipoprotein E (APOE)3/2 genotype and 19 subjects with the APOE3/3 or 3/4 genotype, whose mean7s.d. age was 48714 and 35710 years, respectively. All subjects had normal glucose metabolism. Interventions: The subjects were instructed to increase their sucrose intake by 40 g/day for 8 weeks and to decrease the intake of saturated and unsaturated fat to maintain energy balance. Dietary adherence was monitored using food records and the actual increase in sucrose intake was 39.8718.4 g/day. Sixteen subjects (nine with APOE3/2 genotype, seven with APOE3/3 or 3/4 genotypes) participated also in an 8 h oral fat tolerance test at the beginning and at the end of the intervention. Results: Body weight remained stable during the intervention. Sucrose intake did not have a significant effect on fasting concentrations of serum total and lipoprotein lipids, plasma glucose, serum insulin, squalene and non-cholesterol sterols in either genotype group. Neither were there any changes in postprandial lipid or insulin responses. Conclusions: Moderate increase in sucrose intake does not affect fasting or postprandial serum lipid responses in healthy subjects with or without the e2 allele.

Metabolic Effects of Fructose and the Worldwide Increase in Obesity

“…It was indeed reported that hypertriglyceridemia was related to sucrose consumption only in individuals with the E2 allele (74). These isolated observations were however not confirmed by an intervention study in which subjects were submitted to an increase in dietary sucrose intake of 40 g/day: in these subjects, sucrose supplementation failed to alter fasting or postprandial triglycerides, irrespective of the presence or not of the APOE2 allele (75). The possible relationship between apoE polymorphism and the hypertriglyceridemic effect of fructose/sucrose needs therefore to be further documented by larger studies or with higher dietary intakes.…”

Carbohydrate intake, serum lipids and apolipoprotein E phenotype show association in children

“…In adult CHD patients, the carriers of the E2 have been suggested to be more prone to sucrose‐induced hypertriglyceridaemia (19). However in healthy adults, a moderate increase in sucrose intake did not affect serum lipid responses in those with or without the E2 (27). Further, another study showed that the effect of carbohydrate and dietary fibre intake on serum lipids was similar across apoE genotypes (2).…”

The Effects of Sucrose on Metabolic Health: A Systematic Review of Human Intervention Studies in Healthy Adults

“…They contrasted their results in normal men with those in HTG patients, in whom abnormalities of lipid and glucose metabolism frequently occur together, suggesting that these may not be causally related but rather separate manifestations of a more basic underlying abnormality (Anderson et al, 1973). Another study using a much more modest increase in sucrose intake (by 40 g/day) coupled with a reduced fat intake to maintain energy balance had no effect on fasting plasma glucose, serum insulin, or insulin responses over 8 weeks (Erkkilä et al, 2007). The third study (Brynes et al, 2003) is described in the section “ad libitum studies.”…”