Dataset Information

Paternal under-nutrition programs metabolic syndrome in offspring which can be reversed by antioxidant/vitamin food fortification in fathers.

ABSTRACT: There is an ever increasing body of evidence that demonstrates that paternal over-nutrition prior to conception programs impaired metabolic health in offspring. Here we examined whether paternal under-nutrition can also program impaired health in offspring and if any detrimental health outcomes in offspring could be prevented by micronutrient supplementation (vitamins and antioxidants). We discovered that restricting the food intake of male rodents reduced their body weight, fertility, increased sperm oxidative DNA lesions and reduced global sperm methylation. Under-nourished males then sired offspring with reduced postnatal weight and growth but somewhat paradoxically increased adiposity and dyslipidaemia, despite being fed standard chow. Paternal vitamin/antioxidant food fortification during under-nutrition not only normalised founder oxidative sperm DNA lesions but also prevented early growth restriction, fat accumulation and dyslipidaemia in offspring. This demonstrates that paternal under-nutrition reduces postnatal growth but increases the risk of obesity and metabolic disease in the next generation and that micronutrient supplementation during this period of under-nutrition is capable of restoring offspring metabolic health.

SUBMITTER: McPherson NO

PROVIDER: S-EPMC4891691 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Paternal under-nutrition programs metabolic syndrome in offspring which can be reversed by antioxidant/vitamin food fortification in fathers.

McPherson Nicole O NO Fullston Tod T Kang Wan Xian WX Sandeman Lauren Y LY Corbett Mark A MA Owens Julie A JA Lane Michelle M

Scientific reports 20160603

There is an ever increasing body of evidence that demonstrates that paternal over-nutrition prior to conception programs impaired metabolic health in offspring. Here we examined whether paternal under-nutrition can also program impaired health in offspring and if any detrimental health outcomes in offspring could be prevented by micronutrient supplementation (vitamins and antioxidants). We discovered that restricting the food intake of male rodents reduced their body weight, fertility, increased ...[more]

PMID: 27255552

Similar Datasets

Project description:BackgroundWhile many studies have shown that maternal factors in pregnancy affect the cancer risk for offspring, few studies have investigated the impact of paternal exposures on their progeny's risk of this disease. Population studies generally show a U-shaped association between birthweight and breast cancer risk, with both high and low birthweight increasing the risk compared with average birthweight. Here, we investigated whether paternal malnutrition would modulate the birthweight and later breast cancer risk of daughters.MethodsMale mice were fed AIN93G-based diets containing either 17.7% (control) or 8.9% (low-protein (LP)) energy from protein from 3 to 10 weeks of age. Males on either group were mated to females raised on a control diet. Female offspring from control and LP fathers were treated with 7,12-dimethylbenz[a]anthracene (DMBA) to initiate mammary carcinogenesis. Mature sperm from fathers and mammary tissue and tumors from female offspring were used for epigenetic and other molecular analyses.ResultsWe found that paternal malnutrition reduces the birthweight of daughters and leads to epigenetic and metabolic reprogramming of their mammary tissue and tumors. Daughters of LP fathers have higher rates of mammary cancer, with tumors arising earlier and growing faster than in controls. The energy sensor, the AMP-activated protein kinase (AMPK) pathway, is suppressed in both mammary glands and tumors of LP daughters, with consequent activation of mammalian target of rapamycin (mTOR) signaling. Furthermore, LP mammary tumors show altered amino-acid metabolism with increased glutamine utilization. These changes are linked to alterations in noncoding RNAs regulating those pathways in mammary glands and tumors. Importantly, we detect alterations in some of the same microRNAs/target genes found in our animal model in breast tumors of women from populations where low birthweight is prevalent.ConclusionsOur study suggests that ancestral paternal malnutrition plays a role in programming offspring cancer risk and phenotype by likely providing a metabolic advantage to cancer cells.

Project description:Although social support from fathers is associated with improved child feeding practices, evidence on feasible, acceptable, and effective ways to involve fathers in supporting child nutrition, including animal source food (ASF) consumption, is limited. This study was a follow-on to a trial that tested the effects of social and behavior change communication (SBCC) targeted mainly at mothers to promote ASF consumption by children in households that received an exotic or crossbred cow through the government of Rwanda's Girinka "One Cow Per Poor Family" program (NCT0345567). A delayed SBCC intervention was provided to mothers in the non-intervention arms prior to the present pre/post study, which targeted fathers in households across the trial study arms. Baseline and endline surveys with a cohort of 149 fathers with a child <5 years were used to evaluate the effects of a SBCC intervention for fathers on their children's ASF consumption and on fathers' knowledge, awareness, and support for children's ASF consumption. Qualitative data collected from fathers, mothers, and program implementers were used to assess feasibility and acceptability of the intervention for fathers. The SBCC intervention comprised group meetings led by model fathers, text messages, print materials, and megaphone blasts. The odds of children consuming any type of ASF ≥2 times in the last week increased from baseline to endline (OR 4.9, 95% CI 1.9, 12.3), as did the odds consuming milk, eggs, and beef, but not fish. Fathers' mean ASF knowledge and awareness scores increased from baseline to endline (knowledge: 2.3 to 3.5 out of 4 items, P<0.001; awareness: 2.5 to 3.0 out of 3 items, P<0.001), with the largest changes observed in knowledge of timing of introduction of milk and other ASFs. The percentage of fathers who offered two or more supportive actions for their children's milk and other ASF consumption increased from baseline to endline (milk: 19.5% to 31.5%, P = 0.017; other ASFs: 18.8% to 37.6%, P<0.001). Fathers appreciated gaining knowledge on child nutrition in a setting specifically for men and liked the print materials that offered clear actions they could take to support their children's ASF consumption. This study shows that an SBCC intervention for fathers can improve children's ASF consumption and increase fathers' knowledge, awareness, and support for children's nutrition.

Project description:BackgroundExperimental studies suggest that exposures may impact respiratory health across generations via epigenetic changes transmitted specifically through male germ cells. Studies in humans are, however, limited. We aim to identify epigenetic marks in offspring associated with father's preconception smoking.MethodsWe conducted epigenome-wide association studies (EWAS) in the RHINESSA cohort (7-50 years) on father's any preconception smoking (n = 875 offspring) and father's pubertal onset smoking < 15 years (n = 304), using Infinium MethylationEPIC Beadchip arrays, adjusting for offspring age, own smoking and maternal smoking. EWAS of maternal and offspring personal smoking were performed for comparison. Father's smoking-associated dmCpGs were checked in subpopulations of offspring who reported no personal smoking and no maternal smoking exposure.ResultsFather's smoking commencing preconception was associated with methylation of blood DNA in offspring at two cytosine-phosphate-guanine sites (CpGs) (false discovery rate (FDR) < 0.05) in PRR5 and CENPP. Father's pubertal onset smoking was associated with 19 CpGs (FDR < 0.05) mapped to 14 genes (TLR9, DNTT, FAM53B, NCAPG2, PSTPIP2, MBIP, C2orf39, NTRK2, DNAJC14, CDO1, PRAP1, TPCN1, IRS1 and CSF1R). These differentially methylated sites were hypermethylated and associated with promoter regions capable of gene silencing. Some of these sites were associated with offspring outcomes in this cohort including ever-asthma (NTRK2), ever-wheezing (DNAJC14, TPCN1), weight (FAM53B, NTRK2) and BMI (FAM53B, NTRK2) (p < 0.05). Pathway analysis showed enrichment for gene ontology pathways including regulation of gene expression, inflammation and innate immune responses. Father's smoking-associated sites did not overlap with dmCpGs identified in EWAS of personal and maternal smoking (FDR < 0.05), and all sites remained significant (p < 0.05) in analyses of offspring with no personal smoking and no maternal smoking exposure.ConclusionFather's preconception smoking, particularly in puberty, is associated with offspring DNA methylation, providing evidence that epigenetic mechanisms may underlie epidemiological observations that pubertal paternal smoking increases risk of offspring asthma, low lung function and obesity.

Dataset Information

Paternal under-nutrition programs metabolic syndrome in offspring which can be reversed by antioxidant/vitamin food fortification in fathers.

Publications

Paternal under-nutrition programs metabolic syndrome in offspring which can be reversed by antioxidant/vitamin food fortification in fathers.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets