Similar Datasets
Project description:It is known that both maternal and paternal health/disease can influence the early development and later metabolic homeostasis of the offspring. We investigated whether maternal exercise during gestation alone could protect the offspring from the adverse effects of either maternal or paternal obesity induced by high-fat diet (HFD). To understand the underlying mechanisms we performed transcriptomics, whole-genome DNA methylation and targeted DNA methylation analysis at the metabolic master regulator, peroxisome proliferator-activated receptor g coactivator-1a (Pgc-1a) promoter in the adult offspring skeletal muscle. Both maternal and paternal HFD resulted in impaired glucose tolerance in the offspring at 9 months of age. Maternal exercise during gestation completely mitigated this metabolic impairment induced by either maternal or paternal HFD. Adult offspring exposed to either maternal or paternal HFD without exercise during gestation had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile that was more similar to control offspring from normal chow fed parents. Changes in promoter and CpG DNA methylation were detected between the groups but did not explain the transcriptional changes. Maternal HFD increased methylation of the Pgc-1α promoter at CpG -260, which was prevented by maternal exercise. Paternal HFD did not affect the methylation of the Pgc-1α promoter. These findings demonstrate the negative consequences of maternal and paternal obesity for the offspring’s metabolic outcomes later in life and the clear benefits of maternal exercise during gestation. The mechanisms involve transcriptional regulation of skeletal muscle likely through multiple types of epigenetic modifications.
2021-07-30 | GSE144111 | GEO
Project description:It is known that both maternal and paternal health/disease can influence the early development and later metabolic homeostasis of the offspring. We investigated whether maternal exercise during gestation alone could protect the offspring from the adverse effects of either maternal or paternal obesity induced by high-fat diet (HFD). To understand the underlying mechanisms we performed transcriptomics, whole-genome DNA methylation and targeted DNA methylation analysis at the metabolic master regulator, peroxisome proliferator-activated receptor g coactivator-1a (Pgc-1a) promoter in the adult offspring skeletal muscle. Both maternal and paternal HFD resulted in impaired glucose tolerance in the offspring at 9 months of age. Maternal exercise during gestation completely mitigated this metabolic impairment induced by either maternal or paternal HFD. Adult offspring exposed to either maternal or paternal HFD without exercise during gestation had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile that was more similar to control offspring from normal chow fed parents. Changes in promoter and CpG DNA methylation were detected between the groups but did not explain the transcriptional changes. Maternal HFD increased methylation of the Pgc-1α promoter at CpG -260, which was prevented by maternal exercise. Paternal HFD did not affect the methylation of the Pgc-1α promoter. These findings demonstrate the negative consequences of maternal and paternal obesity for the offspring’s metabolic outcomes later in life and the clear benefits of maternal exercise during gestation. The mechanisms involve transcriptional regulation of skeletal muscle likely through multiple types of epigenetic modifications.
2021-07-30 | GSE144109 | GEO
Project description:Exercise during pregnancy prevents parental obesity-induced decline of metabolic function in adult offspring
| PRJNA602815 | ENA
Project description:Parental health influences embryonic development and susceptibility to disease in the offspring. We investigated whether maternal voluntary running during gestation could protect the offspring from the adverse effects of maternal or paternal high-fat diet (HF) in mice. We performed transcriptomic and whole-genome DNA methylation analyses in female offspring skeletal muscle and targeted DNA methylation analysis of the peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc-1α) promoter in both male and female adult offspring. Maternal HF resulted in impaired metabolic homeostasis in male offspring at 9 mo of age, whereas both male and female offspring were negatively impacted by paternal HF. Maternal exercise during gestation completely mitigated these metabolic impairments. Female adult offspring from obese male or female parent had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile similar to offspring from normal chow (NC)-fed parents. Maternal HF, but not paternal HF, resulted in hypermethylation of the Pgc-1α promoter at CpG-260, which was abolished by maternal exercise. These findings demonstrate the negative consequences of maternal and paternal HF for the offspring's metabolic outcomes later in life possibly through different epigenetic mechanisms, and maternal exercise during gestation mitigates the negative consequences.NEW & NOTEWORTHY Maternal or paternal obesity causes metabolic impairment in adult offspring in mice. Maternal exercise during gestation can completely mitigate metabolic impairment. Maternal obesity, but not paternal obesity, results in hypermethylation of the Pgc-1α promoter at CpG-260, which can be abolished by maternal exercise.
| S-EPMC8091938 | biostudies-literature
Project description:Exercise during pregnancy prevents parental obesity-induced decline of metabolic function in adult offspring [RNA-Seq]
| PRJNA602811 | ENA
Project description:Exercise during pregnancy prevents parental obesity-induced decline of metabolic function in adult offspring [Bisulfite-Seq]
| PRJNA602820 | ENA
Project description:Selenium deficiency during the perinatal period programs metabolic dysfunction in offspring. Postnatal exercise may prevent the development of programmed metabolic disease. This study investigated the impact of selenium deficiency on offspring exercise behavior and whether this improved metabolic health. Female C57BL/6 mice were randomly allocated to control (NormalSe, >190 μg/Se/kg, n = 8) or low-selenium (LowSe, <50 μg/Se/kg, n = 8) diets from four weeks before mating. Male offspring were weaned at postnatal day (PN) twenty-four and placed on a normal chow diet. At PN60, mice were placed in cages with bi-directional running wheels and monitored until PN180. LowSe offspring had a reduced average weekly running speed and distance (p < 0.05). LowSe offspring exhibited glucose intolerance, with increased peak blood glucose (p < 0.05) and area under the curve following an intra-peritoneal injection of glucose (p < 0.05). Furthermore, mRNA expression of several selenoproteins within cardiac and skeletal muscle were increased in LowSe offspring (p < 0.05). The results indicated that selenium deficiency during development reduces exercise behavior. Furthermore, exercise does not prevent programmed glucose intolerance in low-selenium offspring. This highlights that exercise may not be the optimal intervention for metabolic disease in offspring impacted by selenium deficiency in early life.
| S-EPMC8912302 | biostudies-literature
Project description:The intrauterine environment can modulate the course of development and confer an enduring effect on offspring health. The effects of maternal diet to impair offspring metabolic health are well established, but the effects of maternal exercise on offspring metabolic health have been less defined. Because physical exercise is a treatment for obesity and type 2 diabetes (T2D), maternal exercise is an appealing intervention to positively influence the intrauterine environment and improve the metabolic health of offspring. Recent research has provided insights into the effects of maternal exercise on the metabolic health of adult offspring, which is the focus of this review.
| S-EPMC5826804 | biostudies-literature
Project description:Obesity in the western world has reached epidemic proportions, and yet the long-term effects on brain health are not well understood. To address this, we performed transcriptional profiling of brain regions from a mouse model of western diet (WD)-induced obesity. Both the cortex and hippocampus from C57BL/6J (B6) mice fed either a WD or a control diet from 2 months of age to 12 months of age (equivalent to midlife in a human population) were profiled. Gene set enrichment analyses predicted that genes involved in myelin generation, inflammation, and cerebrovascular health were differentially expressed in brains from WD-fed compared to control diet-fed mice. White matter damage and cerebrovascular decline were evident in brains from WD-fed mice using immunofluorescence and electron microscopy. At the cellular level, the WD caused an increase in the numbers of oligodendrocytes and myeloid cells suggesting that a WD is perturbing myelin turnover. Encouragingly, cerebrovascular damage and white matter damage were prevented by exercising WD-fed mice despite mice still gaining a significant amount of weight. Collectively, these data show that chronic consumption of a WD in B6 mice causes obesity, neuroinflammation, and cerebrovascular and white matter damage, but these potentially damaging effects can be prevented by modifiable risk factors such as exercise.
| S-EPMC7846054 | biostudies-literature
Project description:The intrauterine environment during pregnancy is a critical factor in the development of diabetes and obesity in offspring. To determine the effects of maternal exercise during pregnancy on the metabolic health of offspring, 6-week-old C57BL/6 virgin female mice were fed a chow (21%) or high-fat (60%) diet and divided into four subgroups: trained (housed with running wheels for 2 weeks preconception and during gestation), prepregnancy trained (housed with running wheels for 2 weeks preconception), gestation trained (housed with running wheels during gestation), or sedentary (static cages). Male offspring were chow fed, sedentary, and studied at 8, 12, 24, 36, and 52 weeks of age. Offspring from chow-fed dams that trained both before and during gestation had improved glucose tolerance beginning at 8 weeks of age and continuing throughout the 1st year of life, and at 52 weeks of age had significantly lower serum insulin concentrations and percent body fat compared with all other groups. High-fat feeding of sedentary dams resulted in impaired glucose tolerance, increased serum insulin concentrations, and increased percent body fat in offspring. Remarkably, maternal exercise before and during gestation ameliorated the detrimental effect of a maternal high-fat diet on the metabolic profile of offspring. Exercise before and during pregnancy may be a critical component for combating the increasing rates of diabetes and obesity.
| S-EPMC4303966 | biostudies-literature