Journal of Developmental Origins of Health and Disease最新文献

The aim of this study is to determine if the offspring of mothers with obesity, present disorders in the expression of genes related to atrophy or protein synthesis in the muscle and if these disorders are modified with the (-)-epicatechin (Epi) treatment. Six male offspring per group were randomly assigned to the control groups [C and offspring of maternal obesity (MO)] or the Epi intervention groups, Epi treatment for 13 weeks (C + Epi long or MO + Epi long), or Epi administration for two weeks (C + Epi short or MO + Epi short). The effect of Epi in the gastrocnemius tissue was evaluated, analyzing mRNA and protein levels of Murf1, MAFbx, Foxo1, NFkB, and p70S6K-alpha. After the analysis by two-way ANOVA, we found an influence of the Epi long treatment over the model, by decreasing the Murf1 gene expression in both groups treated with the flavonoid (C + Epi long and MO + Epi long) (p = 0.036). Besides, Epi long treatment over the NFκB expression, by decreasing the fold increase in both groups treated with the flavonoid (C + Epi long and MO + Epi long) (p = 0.038). We not find any interaction between the variables or changes in the MAFbx, Foxo1 mRNA, neither in the phosphorylated/total protein ratio of NFκB, Foxo1, or p70S6K-alpha. In conclusions, treatment with a long protocol of Epi, reduces the mRNA of the muscle atrophy genes Murf 1 and NFkB, in the gastrocnemius muscle; however, these changes are not maintained at protein level.

The global surge in childhood obesity is also evident in Indonesia. Parental body mass index (BMI) values were found to be one of the major determinants of the increasing prevalence of childhood obesity. It is uncertain if parental BMI during their offspring's childhood significantly affects their children's BMI trajectories into adulthood. We aimed to investigate the influence of parental BMI Z-scores on BMI trajectories of Indonesian school-aged children, with a focus on sex-specific effects. This study utilized data from the Indonesian Family Life Survey and tracked the same respondents over four time points, from wave 2 (1997-1998) to wave 5 (2014-2015). The sample of this study consisted of children aged 5-12 years in wave 2 for whom height and weight data were available. We utilized a two-level growth curve model to account for the hierarchical structure of the data, with time nested within individual children. Fathers' BMI Z-scores in wave 2 had a pronounced influence (β = 0.31) on female children's BMI Z-scores compared to the influence of mothers' BMI Z-scores (β = 0.17). Mothers' BMI Z-scores in wave 2 showed a stronger positive association with male children's BMI Z-scores (β = 0.22) than did the father's BMI Z-scores (β = 0.19). A significant interaction of fathers' BMI Z-scores and years of follow-up was found for male children. As male children's BMI Z-scores increased by year, this effect was stronger in those whose fathers' BMI Z-scores were at a higher level. In conclusion, we found that parental BMI values profoundly influenced their children's BMI trajectories.

In mammals, DNA methylation (DNAme) erasure and reinstatement during embryo development and germline establishment are sensitive to the intrauterine environment. Maternal intake of a high-fat diet (HFD), associated with excessive gestational weight gain, has transgenerational effects on offspring health, which may be mediated by changes in DNAme in the germline. Here, we tested the impact of a maternal HFD on embryonic germline DNAme erasure using a rat strain that expresses green fluorescent protein specifically in germ cells. DNAme was analysed by methyl-seq capture in germ cells collected from male and female F1 gonads at gestational day 16. Our data show that although HFD induced global hypomethylation in both sexes, DNAme erasure in female germ cells was more advanced compared to male germ cells. The delay in DNAme erasure in males and the greater impact of HFD suggest that male germ cells are more vulnerable to alterations by exogenous factors.

Over the last few years, during the pandemic, the Brazilian population has suffered several problems, ranging from health to socioeconomic impacts. When we consider Brazilian science, there has been an undeniable scientific delay generated by the pandemic, especially in areas that are not related to the coronavirus. In this context, with the aim of fostering collaboration among researchers in the field of Developmental Origins of Health and Diseases (DOHaD) and enhancing the potential for implementing public health strategies to prevent noncommunicable chronic diseases, the Brazilian Association of Developmental Origins of Health and Diseases (DOHaD Brazil) was established in 2020. In this narrative, we explore the effects of the COVID-19 pandemic in Brazil, focusing on its impacts on scientific research conducted in universities. Additionally, we underscore the significance of the DOHaD Brazil Association, particularly from the perspective of young researchers engaged in DOHaD research in Brazil.

This study aimed to determine if maternal fatty acids (FA) levels during pregnancy are associated with the occurrence of neural tube defects (NTDs) and to explore the correlation between FA and maternal vitamin D, homocysteine, vitamin B₁₂, and folate in cases. Plasma FA composition was assessed using capillary gas chromatography. Comparisons between cases and controls were performed by independent samples t-test for continuous variables. Cases had significantly higher levels of heptadecanoic acid, linolelaidic acid, and arachidonic acid (ARA):(eicosapentaenoic acid+docosahexaenoic acid) ratio than controls (p < 0.05). Nervonic acid, ARA, adrenic acid, eicosapentaenoic acid, docosahexaenoic acid, and omega-3 polyunsaturated fatty acids (n-3 PUFA) levels were significantly lower in cases (p < 0.05). Maternal 25-hydroxyvitamin D (25(OH)D) levels were positively correlated with maternal polyunsaturated fatty acids and omega-6 polyunsaturated fatty acids. RBC folate levels were negatively correlated with n-3 PUFA.Further research is required to clarify the association of FA metabolism with NTDs.

Early-life family meal participation has been associated with several aspects of nutritional health, but longitudinal associations with linear growth have not yet been investigated. The aim of this study was to investigate whether family meal participation at 12 months of age associates with anthropometric measures 3 years later. We used follow-up data from children born to mothers in the Norwegian Fit for Delivery trial (NFFD) and included 368 first-borns with dietary and anthropometric data at 12 months and 4 years of age. We treated the sample as a cohort and conducted subgroup analyses by randomization status. A family meal participation score was used as exposure, and weight, height, and body mass index (BMI) as outcomes in crude and multivariable linear regression models adjusted for maternal education, randomization status, and child sex.Higher family meal participation score at 12 months was positively associated with length at 12 months (B = 0.198, 95% CI 0.028, 0.367, p = 0.022) and 4 years (B = 0.283, 95% CI 0.011, 0.555, p = 0.042) in multivariable models. After additional adjustment for maternal height the associations attenuated and were no longer significant. An inverse association with BMI at 4 years of age was observed in children born to mothers that had been exposed to the NFFD intervention (B = -0.144, 95% CI -0.275, -0.014, p = 0.030), but attenuated after adjustment for maternal BMI.The longitudinal association observed between early family meal participation and child height was largely explained by maternal height. The relationship with BMI differed according to maternal participation in a lifestyle intervention trial during pregnancy.

Obesity is associated with osteoarthritis (OA), but few studies have used fetal origin to explore the association. Our study aims to disentangle the causality between birth weight, childhood obesity, and adult OA using Mendelian randomization (MR). We identified single nucleotide polymorphisms (SNPs) related to birth weight (n = 298,142) and childhood obesity (n = 24,160) from two genome-wide association studies contributed by the Early Growth Genetics Consortium. Summary statistics of OA and its phenotypes (knee, hip, spine, hand, thumb, and finger OA) from the Genetics of Osteoarthritis Consortium (n = 826,690) were used to estimate the effects of SNPs on OA. Multivariable MR (MVMR) was conducted to investigate the independent effects of exposures. It turned out that genetically predicted standard deviation increase in birth weight was not associated with OA. In contrast, there was a marginally positive effect of childhood obesity on total [odds ratio (OR) = 1.07, 95% confidence interval (CI) = 1.00, 1.15 using IVW], knee (OR = 1.13, 95% CI = 1.05, 1.22 using weighted median), hip (OR = 1.13, 95% CI = 1.04, 1.24 using IVW), and spine OA (OR = 1.12, 95% CI = 1.03, 1.22 using IVW), but not hand, thumb, or finger OA. MVMR indicated a potential adulthood body mass index-dependent causal pathway between childhood obesity and OA. In conclusion, no association of birth weight with OA was suggested. Childhood obesity, however, showed a causality with OA in weight-bearing joints, which seems to be a general association of obesity with OA.