Background: There seems to be a consensus that family influences on dietary habits are important. However, no data relative to breakfast have been published yet. Objective: To investigate whether and how breakfast energy intake aggregates within French families. Design: A total of 398 families of the Stanislas Family Study who filled in a 3 day food consumption diary were selected. Absolute and relative breakfast energy intakes (BEI in kcal=day and RBEI in percentage of daily intake, respectively) were both studied. Results: By using a variance component analysis, no genetic influence was shown in family aggregation of both BEI and RBEI. Intra-generation common environmental contribution to total phenotypic variance of BEI and RBEI was higher than intergeneration; both were increased with frequency of sharing breakfast. Furthermore frequency of sharing breakfast contributed to increase family resemblance in breakfast energy intake, particularly in offspring for BEI and RBEI, and in spouses for RBEI. Smoking habits, alcohol consumption, BMI or physical activity were related to family resemblance, but after adjustment on each factor degrees of resemblance were almost unchanged. Conclusion: General findings of this study were that family aggregation in breakfast absolute and relative energy intakes was significant within Stanislas families. Family resemblance depended on inter-and intra-generation components and was modified by the number of shared breakfasts. Our study confirmed that familial habits act on family resemblance in both absolute and relative breakfast energy intakes, so that family should be a favorite unit for health and diet promotion programs.
The aim was to study the mechanisms involved in the dyslipidemia associated with lipodystrophy in HIV infected patients on antiretroviral therapy (ART). We investigated the in vivo kinetics of apolipoprotein B100 (apoB) containing lipoproteins using a 14 h primed constant infusion of [5,5,5, (2)H(3)] leucine and compartmental modelling in normolipidemic without lipodystrophy (7 patients, NLD) or dyslipidemic with lipodystrophy (7 patients, LD) treated with ART. Subjects in group LD showed higher plasma triglycerides (5.73+/-3.58 vs 1.29+/-0.54 g/L, p<0.005), total cholesterol (2.98+/-0.95 vs 1.74+/-0.26 g/L, p<0.05), apoB (1.49+/-1.11 vs 0.51+/-0.11 g/L, p<0.005) and apolipoprotein CIII in apoB containing lipoproteins (117.7+/-42.2 vs 22.6+/-23.9 g/L, p<0.005). LD subjects exhibited an insulin resistant as observed by higher HOMA (3.44+/-1.62 vs 1.60+/-0.61, p<0.05). They exhibited an increase in VLDL (1.24+/-0.33 vs 0.80+/-0.21 mg/kg/h, p<0.05), decrease in IDL (0.20+/-0.10 vs 0.48+/-0.24 mg/kg/h, p<0.05) and no difference in LDL (0.38+/-0.19 vs 0.45+/-0.25 mg/kg/h) production rate. LD subject also showed a dramatic decrease in transformation of VLDL to IDL (0.013+/-0.010 vs 0.258+/-0.206 h(-1), p<0.005) and IDL to LDL (0.088+/-0.093 vs 0.366+/-0.189 h(-1), p<0.05) and a decrease in fractional catabolic rate (FCR) of VLDL (0.199+/-0.132 vs 0.555+/-0.398 h(-1), p<0.05), IDL (0.110+/-0.08 vs 0.523+/-0.275 h(-1), p<0.05) and LDL (0.010+/-0.005 vs 0.025+/-0.014 h(-1), p<0.05). These disturbances, overproduction and an overall delayed catabolism of apoB, are similar to those observed using the same protocol in insulin resistant subjects. Our study suggests that metabolic disturbance of apoB100 observed in lipodystrophic HIV in combined antiretroviral therapy are consecutive to insulin resistance induced by the treatment.
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