The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase, which led to impaired triacylglycerol clearance. The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small, but its effect on altering the partitioning of fatty acids toward esterification may be considerable.

Integrating the genotype with epigenetic marks holds the promise of better understanding the biology that underlies the complex interactions of inherited and environmental components that define the developmental origins of a range of disorders. The quality of the in utero environment significantly influences health over the lifecourse. Epigenetics, and in particular DNA methylation marks, have been postulated as a mechanism for the enduring effects of the prenatal environment. Accordingly, neonate methylomes contain molecular memory of the individual in utero experience. However, interindividual variation in methylation can also be a consequence of DNA sequence polymorphisms that result in methylation quantitative trait loci (methQTLs) and, potentially, the interaction between fixed genetic variation and environmental influences. We surveyed the genotypes and DNA methylomes of 237 neonates and found 1423 punctuate regions of the methylome that were highly variable across individuals, termed variably methylated regions (VMRs), against a backdrop of homogeneity. MethQTLs were readily detected in neonatal methylomes, and genotype alone best explained~25% of the VMRs. We found that the best explanation for 75% of VMRs was the interaction of genotype with different in utero environments, including maternal smoking, maternal depression, maternal BMI, infant birth weight, gestational age, and birth order. Our study sheds new light on the complex relationship between biological inheritance as represented by genotype and individual prenatal experience and suggests the importance of considering both fixed genetic variation and environmental factors in interpreting epigenetic variation.

Parallel activation of DNL and SCD was found after a short period of HC feeding.

Higher maternal folate coupled with vitamin B12 insufficiency was associated with higher GDM risk. This finding has potential implications for antenatal supplement recommendations but will require confirmation in future studies.

Metabolic alterations suggestive of repartitioning of fatty acids away from oxidation toward esterification in both liver and muscle occur in response to short-term adaptation to a HC diet.

BackgroundAppetitive traits in childhood such as food responsiveness and enjoyment of food have been associated with body mass index (BMI) in later childhood. However, data on appetitive traits during infancy in relation to BMI in later childhood are sparse. We aimed to relate appetitive traits in infancy to subsequent BMI and weight gain up to 24 months of age.MethodsData of 210 infants from the Singapore GUSTO mother-offspring cohort was obtained. The Baby Eating Behavior Questionnaire (BEBQ) and the Child Eating Behavior Questionnaire (CEBQ) were administered to mothers when their offspring were aged 3 and 12 months respectively. Height and weight of offspring were measured at ages 3, 6, 9,12,15,18 and 24 months. The association of appetitive traits with both BMI z-score and weight gain were evaluated using multivariate linear regression.ResultsFood responsiveness at 3 months was associated with higher BMI from 6 months up to 15 months of age (p < 0.01) and with greater weight gain between 3 and 6 months of age (p = 0.012). Slowness in eating and satiety responsiveness at 3 months was significantly associated with lower BMI at 6 months (p < 0.01) and with less weight gain between 3 to 6 months of age (p = 0.034). None of the appetitive traits at 12 months were significantly associated with BMI or weight gain over any time period.ConclusionEarly assessment of appetitive traits at 3 months of age but not at 12 months of age was associated with BMI and weight gain over the first two years of life.Trial registrationClinical Trials identifier NCT01174875Electronic supplementary materialThe online version of this article (doi:10.1186/s12887-015-0467-8) contains supplementary material, which is available to authorized users.

Epidemiological studies suggest that high intakes of dietary flavonoids are associated with decreased cardiovascular disease mortality and risk factors. Less is known about the cardioprotective effects of flavonoids from fruit and vegetables. This review summarizes data from studies which examine the effects of commonly consumed fruit and vegetables on cardiovascular disease risk biomarkers in healthy volunteers or at-risk individuals. Although flavonoids from apples, berries, and onions appear to impact positively on blood pressure, vascular function, and serum lipid levels, further research is required to find out the optimal quantity and food matrix for conferring substantial clinical benefit. The benefits from citrus flavonoids are still inconclusive. Further robust, longer-term dietary intervention studies, with the inclusion of placebo or control arms, are required to improve the credibility of the findings and confirm current observations. An improved understanding of the impact of flavonoids from fruit and vegetables can help one make discerning food choices for optimal cardiovascular health.

The elevation of blood lipid concentrations in response to the consumption of low-fat high-carbohydrate diets is known as carbohydrate-induced hypertriacylglycerolaemia (HPTG). An understanding of the mechanisms involved in the interaction between carbohydrates and plasma lipids may help determine whether carbohydrate-induced HPTG would increase cardiovascular risk. There is growing evidence to suggest that the sugar component of the diet may be largely responsible, rather than the total carbohydrate. In most studies designed to investigate the mechanisms of carbohydrate-induced HPTG, the amounts and types of sugars and starches used in the diets are not specified. Findings have been mixed and inconsistent. It is proposed that the elucidation of mechanisms from current studies could have been confounded by the different ways in which sugars are metabolized in the body. At present, there are few studies that have evaluated the independent effects of dietary sugars. Interest has been focused onde novolipogenesis (DNL), as it has recently been found to be positively correlated with increases in fasting TAG levels produced on high-carbohydrate diets, indicating that DNL may contribute to carbohydrate-induced HPTG. DNL has been found to be determined by starch:sugar in a high-carbohydrate diet and affected by different types of sugars. The presence of DNL in adipose tissue is supported by emerging gene-expression studies in human subjects. In the wake of rising intakes of sugars, further research is needed to investigate the mechanisms associated with different sugars, so that appropriate therapeutic strategies can be adopted.