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Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model

ABSTRACT: Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model

PROVIDER: PRJNA471320 | ENA |

REPOSITORIES: ENA

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Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (MBD-seq)

Project description:Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (MBD-seq)

| PRJNA471326 | ENA

Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (small RNA-seq)

Project description:Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (small RNA-seq)

| PRJNA471323 | ENA

Paternal malnutrition programs breast cancer risk and tumor metabolism in offspring.

Project description: Not available

| S-EPMC6117960 | biostudies-literature

Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-06-14 | GSE114423 | GEO

Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (MBD-seq)

Project description:We found that LP daughters have lower birthweight, alterations in mammary gland morphology and higher rates of mammary cancer. Further, we found that mammary glands and tumors of LP daughters are metabolic rewired, with alterations in the AMPK and amino-acid metabolism pathways. These changes were associated with differential expression of miRNAs 451a, miR-200c and miR-92a. Importantly, some of the same miRNAs and target genes alterations were detected in breast tumors of women from populations with high rates of low birthweight.

2018-06-14 | GSE114422 | GEO

Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (small RNA-seq)

2018-06-14 | GSE114421 | GEO

Rapid increase of fibroblast growth factor 21 under protein malnutrition and its impact on growth and lipid metabolism

Project description:Protein malnutrition promotes hepatic steatosis, decreases insulin-like growth factor (IGF)-I production, and retards growth. In order to identify new molecules involved in such changes, we conducted DNA microarray analysis for liver samples of rats fed isoenergetic low protein diet for 8 hours, and identified fibroblast growth factor 21 (Fgf21) as one of the most strongly up-regulated genes under conditions of acute protein malnutrition (P<0.05, FDR<0.001). In addition, amino acid deprivation from the culture media increased Fgf21 mRNA levels in rat liver-derived RL-34 cells (P<0.01). Thus, it was suggested that amino acid limitation directly increases Fgf21 expression. FGF21 is a polypeptide hormone that regulates glucose and lipid metabolism. Using transgenic mice, FGF21 has also been shown to promote a growth hormone-resistant state and suppress IGF-I. Therefore, to further determine whether the up-regulation of Fgf21 under protein malnutrition causes hepatic steatosis and growth retardation following decrease in IGF-I, we fed isoenergetic low protein diet to Fgf21-knockout (KO) mice. Fgf21-KO did not rescue growth retardation and reduced plasma IGF-I concentration of mice fed the low-protein diet. Meanwhile, Fgf21-KO mice showed greater epididymal white adipose tissue weight as well as hepatic triglyceride and cholesterol levels under protein malnutrition (P<0.05). Taken together, we showed that protein deprivation directly increases Fgf21 expression. However, growth retardation and decreased IGF-I were not mediated by increased FGF21 expression under protein malnutrition. Furthermore, up-regulated FGF21 rather appears to have a protective effect against obesity and hepatic steatosis in protein malnourished animals. Livers of rats from 2 groups (control (15P) or low-protain (5P) diet fed groups), total of 6 samples (3 replicates for each group) were analyzed.

2015-01-15 | E-GEOD-64970 | biostudies-arrayexpress

Microbes Malnutrition Microglia

Project description:Microbes Malnutrition Microglia

| PRJNA575001 | ENA

Paternal microbiome perturbations impact offspring fitness

Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is not explored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birthweight, severe growth restriction, and premature mortality. Paternal transmission of disease risk is provoked by pervasive microbiome perturbations, including (non)-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the gut microbiota prior to conception. This reflects a dynamic male reproductive response to induced dysbiosis, that includes impaired leptin signalling, an altered metabolite and physiological configuration in testes, and remapped small RNA payloads in sperm. As a result, dysbiotic males trigger in utero placental insufficiency, which exhibits hallmarks of pre-eclampsia, and reveals a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, that is sensitive to environmental exposures, and programs offspring fitness through impacting placental function. </p>

2024-02-12 | MTBLS1629 | MetaboLights

Transcriptomic analysis of paternal behaviors in prairie voles

Project description:The importance of fathers' engagement in care and its critical role in the offspring’s cognitive and emotional development is now well established. Yet, little is known on the underlying neurobiology due to the lack of appropriate animal models. In the socially monogamous and bi-parental prairie vole (Microtus ochrogaster), while most virgin males show spontaneous paternal behaviors (Paternal), others display pup-directed aggression (Attackers). Here we took advantage of this phenotypic dichotomy and used RNA-sequencing in three important brain areas to characterize gene expression associated with paternal behaviors of Paternal males and compare it to experienced fathers and mothers. This strategy allowed the identification of spontaneous paternal behaviors independently from fatherhood and pair-bonding. While Paternal males displayed the same range and extent of paternal behaviors than experienced Fathers, the nucleus accumbens (NAc) and medial preoptic area (MPOA) transcriptomes mainly reflected pair-bonded status or sex differences, respectively. The lateral septum (LS) transcriptome, however, primarily reflected phenotypic differences between Paternal and Attackers and suggested the involvement of the mitochondria, RNA translation, and protein degradation processes. Altogether, these observations highlight a marked structure- and phenotype-specific pattern of gene expression underlying paternal behaviors in prairie voles and highlight similarities and differences from those underlying fatherhood.

2022-10-05 | GSE190213 | GEO

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