RNA-mediated paternal heredity of diet-induced obesity and type II diabetes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE44301 | GEO | 2013/02/14
SECONDARY ACCESSION(S): PRJNA189406
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression analysis of testis RNA obtained from mice fed on High Fat and Standard diets. The aim of the study is to identify differentially expressed transcript in testis of the obese males which might be involved in the RNA-mediated paternal heredity of diet-induced obesity and typeII diabete Total RNA obtained from testis of mice fed on High Fat and standard diets
2013-02-14 | E-GEOD-44301 | biostudies-arrayexpress
Project description:Epidemiological surveys first indicated that obesity and type II diabetes generated by lipid rich diets may be efficiently inherited, both paternally and maternally. This apparent exception to the fundamental law of non heritability of acquired characters was more recently documented in laboratory organisms but the transgenerational signal remained a matter of speculation. Here we show that experimental transfer to healthy one-cell embryos of testis RNA prepared from males raised on high-fat-diet (HFD) results in the development of obesity and diabetes in the adult. Body weight, fasting glucose levels, response to insulin, glucose tolerance, RNA levels of leptin and stearoyl-CoA desaturase were all affected in mice born after RNA microinjection to the same extent as in the progenitors and in their sexual offspring. Surprisingly, neither microarray hybridization nor deep sequencing of the inducer and control RNAs showed a differential expression of known regulators of adipogenesis, but only modest variations in a series of transcripts. Transgenerational maintenance appears as one instance of the RNA-mediated heredity of epigenetic traits previously demonstrated in experimental systems ranging from the worm to the mouse. The relationship between lipid-rich diet and changes in testicular RNAs on one side and the nature of the mark imprinted on the one-cell embryo by RNA transfer and responsible for pathological developments at later stages are questions of interest for future studies. Two experimental groups composed of four individuals. Controls = M1N,M2N,TN1,TN2 and Experimentals= M1W,M2W,M3W,M5W.
2014-01-16 | E-GEOD-43555 | biostudies-arrayexpress
Project description:Epidemiological surveys first indicated that obesity and type II diabetes generated by lipid rich diets may be efficiently inherited, both paternally and maternally. This apparent exception to the fundamental law of non heritability of acquired characters was more recently documented in laboratory organisms but the transgenerational signal remained a matter of speculation. Here we show that experimental transfer to healthy one-cell embryos of testis RNA prepared from males raised on high-fat-diet (HFD) results in the development of obesity and diabetes in the adult. Body weight, fasting glucose levels, response to insulin, glucose tolerance, RNA levels of leptin and stearoyl-CoA desaturase were all affected in mice born after RNA microinjection to the same extent as in the progenitors and in their sexual offspring. Surprisingly, neither microarray hybridization nor deep sequencing of the inducer and control RNAs showed a differential expression of known regulators of adipogenesis, but only modest variations in a series of transcripts. Transgenerational maintenance appears as one instance of the RNA-mediated heredity of epigenetic traits previously demonstrated in experimental systems ranging from the worm to the mouse. The relationship between lipid-rich diet and changes in testicular RNAs on one side and the nature of the mark imprinted on the one-cell embryo by RNA transfer and responsible for pathological developments at later stages are questions of interest for future studies.
2014-01-16 | GSE43555 | GEO
Project description:Gene expression analysis of sperm small RNA obtained from mice fed either a control or Western diets for one or five successive generations through the paternal lineage. The aim of the study is to identify differentially expressed small RNA in sperm of obese males which might be involved in the long-term epigenetic inheritance of obesity induced by the maintenance of High Fat Diet feeding for 5 successive generations.
2021-03-31 | GSE138989 | GEO
Project description:The global rise in obesity has revitalized a search to understand genetic, and in particular, epigenetic factors underlying the disease. We present a Drosophila model of paternal-diet-induced Inter-Generational Metabolic Reprogramming (IGMR) and identify genes required for its encoding in offspring. Intriguingly, we find that as little as two days of dietary intervention in fathers elicits obesity in offspring. Paternal sugar acts as a physiological suppressor of variegation, de-silencing chromatin state-defined transcriptional units in both mature sperm and in offspring embryos. We identify requirements for H3K9/K27me3 dependent reprogramming of metabolic genes in two distinct germline and zygotic windows. Critically, we find evidence that a similar system regulates obesity-susceptibility and phenotype variation in mice and humans. The findings provide insight into the mechanisms underlying intergenerational metabolic reprogramming and carry profound implications for our understanding of phenotypic variation and evolution. RNA-seq on Drosophila embryos and sperm samples fed medium and high sugar.
2014-12-04 | E-GEOD-62668 | biostudies-arrayexpress
Project description:The global rise in obesity has revitalized a search to understand genetic, and in particular, epigenetic factors underlying the disease. We present a Drosophila model of paternal-diet-induced Inter-Generational Metabolic Reprogramming (IGMR) and identify genes required for its encoding in offspring. Intriguingly, we find that as little as two days of dietary intervention in fathers elicits obesity in offspring. Paternal sugar acts as a physiological suppressor of variegation, de-silencing chromatin state-defined transcriptional units in both mature sperm and in offspring embryos. We identify requirements for H3K9/K27me3 dependent reprogramming of metabolic genes in two distinct germline and zygotic windows. Critically, we find evidence that a similar system regulates obesity-susceptibility and phenotype variation in mice and humans. The findings provide insight into the mechanisms underlying intergenerational metabolic reprogramming and carry profound implications for our understanding of phenotypic variation and evolution.
2014-12-04 | GSE62668 | GEO
Project description:Long noncoding RNAs could act as vectors for paternal heredity of high fat diet-induced obesity
| PRJNA484175 | ENA
Project description:Background: Defining the mechanisms that establish and regulate the transmission of epigenetic information from parent to offspring is critical for understanding disease heredity. Currently, the molecular pathways that regulate epigenetic information in the germline and its transmission to offspring are poorly understood. Results: Here we provide evidence that Polycomb Repressive Complex 2 (PRC2) regulates paternal inheritance, both at the phenotypic and molecular levels. Reduced PRC2 function in mice resulted in male sub-fertility and altered epigenetic and transcriptional control of retrotransposed elements in fetal male germ cells. Males with reduced PRC2 function produced offspring that over-expressed retrotransposed pseudogenes and had altered preimplantation embryo cleavage rates and cell cycle control. Conclusion: This study reveals a novel role for the histone modifying complex, PRC2, in epigenetic inheritance, with important implications for understanding disease inheritance.
2018-02-15 | GSE110529 | GEO
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
Project description:Epidemiological studies suggest that a father’s diet can influence offspring health. A proposed mechanism for paternal transmission of environmental information is via the sperm epigenome. The epigenome includes heritable information such as DNA methylation. We hypothesized that the dietary supply of methyl donors would alter epigenetic reprogramming in sperm. This hypothesis was examined by feeding male mice a folate deficient (FD) and folate sufficient (FS) diets and then generating and analyzing DNA methylation profiles of their sperm. C57BL/6 males were fed either the FS or FD diet throughout life (FS, n=32; FD, n=35; 2-3 month old). Pooled gene promoter DNA methylation profiles were generated from the sperm of three FS males and four FD males using the method of MeDIP (Methylated DNA Immunoprecipitation) followed by microarray hybridization.
2013-11-02 | E-GEOD-52017 | biostudies-arrayexpress