Authors | Umpleby, M., Shojaee-Moradie, F., Fielding, B., Li, X., Isherwood, C., Jackson, N., Wilinska, G., Hovorka, R., Bell, J., Thomas, E. L., Wright, J., Frost, G. S. and Griffin, B. |
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Abstract | Aim: To determine how dietary sugar promotes the formation of an atherogenic lipoprotein phenotype by studying the effects of high and low sugar diets on lipoprotein kinetics. Methods: Two groups of men at risk of metabolic syndrome, with low liver fat (LLF; <5%) (n=14) or high liver fat (HLF; >5%) [BAG1] (n=11), were randomised to a cross-over intervention with high and low sugar diets (HSD; 26% energy or LSD; 6% energy) for 12 weeks. ApoB production (PR) and fractional catabolic rates (FCR) of lipoprotein fractions (VLDL1, VLDL2, IDL, LDL2 and LDL3 apolipoproteinB (apoB)) were measured by constant infusion of 13C-leucine and mathematical modelling. Results: In post-dietary comparisons (LSD v HSD), liver fat was lower after the LSD in both groups (HLF, p=0.01; LLF, p=0.008). In LLF men, VLDL1 apoB, TG and cholesterol concentration, LDL3 apoB concentration and VLDL1 apoB PR were lower (all p <0.05) after a LSD whilst VLDL1 apoB FCR and VLDL2, IDL and LDL apoB kinetics were not different. In HLF men, plasma TG was lower (p<0.04), but VLDL1 and VLDL2 apoB kinetics were unchanged after the LSD but IDL apoB, TG and cholesterol concentration, IDL apoB PR and LDL3 apoB PR and FCR were lower (All p=0.05). Small dense LDL cholesterol and oxidized LDL were lower in both groups after the LSD (HLF: p=0.02, p=0.08; LLF: p=0.02, p<0.02 respectively). Conclusion: Men with HLF and LLF respond differently to dietary sugar. A LSD can reduce the production of atherogenic lipoproteins in men with HLF. |
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