RESUMEN
An alternative approach in determining cause, treatment, and prevention of obesity is to study those who appear resistant to the obesogenic environment. We examined appetite responses in 33 obesity resistant individuals (ORI) versus 28 obesity susceptible individuals (OSI). Fingerprick blood samples to measure ghrelin, total peptide YY (PYY), leptin, glucose, and insulin along with appetite ratings were collected at baseline and 15, 30, 60, 120, and 180 min following consumption of a standardized meal. Fasting, area under the curve (AUC), peak/nadir, and time to peak/nadir were compared. Participants completed the three factor eating questionnaire (TFEQ). No significant differences were observed for ghrelin or PYY. Higher leptin concentrations in the OSI disappeared after controlling for percent body fat (%BF). Significant differences in appetite ratings included a lower hunger nadir among OSI compared with ORI (P = 0.017). Dietary restraint (P < 0.001) and disinhibition (P < 0.001) were lower in ORI compared with OSI, with and without adjustment for %BF. Given the differential body weight of the study groups, similar observed ghrelin concentrations were unexpected, perhaps indicating OSI and ORI respond differently to the same ghrelin concentration. Also ORI response to hunger appears different as they exhibit lower levels of dietary restraint and disinhibition compared with OSI.
RESUMEN
BACKGROUND AND AIMS: Some individuals respond to a greater extent than others to changes in dietary fat and cholesterol even when dietary intake is consistent. A prospective study has been undertaken in which two groups of individuals according to cholesteryl ester transfer protein (CETP) genotype were compared in terms of plasma lipid response to altering the nature of dietary fat in a free-living situation. METHODS AND RESULTS: Following genotyping, 35 individuals with the CETP Taq1 B1B1 genotype were paired with age and sex-matched individuals with one or two CETP B2 alleles, to undertake a single crossover trial with a diet high in saturated fat and a diet high in polyunsaturated fat. There was no washout period between the two 4-week phases. Plasma lipoproteins were measured at the beginning and end of each phase. The difference (95% CI) in plasma LDL-cholesterol concentration at the end of the PUFA and SAFA diets was 0.95 (0.71, 1.19) mmol/l in the CETP B1B1 group and 0.80 (0.57, 1.04) mmol/l in the group with at least one CETP B2 allele. The dietary induced changes in the two genotype groups were not significantly different (p=0.38) from each other. Comparable results were observed for plasma total cholesterol. The high PUFA and SAFA diets did not significantly alter plasma HDL concentration in either of the CETP genotype groups. Response was also similar according to apolipoprotein E genotype (E3E3 vs E4+) and lipoprotein lipase genotype (S447X). CONCLUSIONS: The results of this study do not support previous studies in which CETP genotype predicted plasma LDL-cholesterol response to diet. CETP genotype does not significantly affect the change in plasma total and LDL-cholesterol concentrations that occur when altering the nature of dietary fat. These data suggest that the influence of genetic factors on total and LDL-cholesterol may be relatively small in comparison with the effect of dietary manipulation.