Long noncoding RNAs could act as vectors for paternal heredity of high fat diet-induced obesity
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PROVIDER: PRJNA484175 | ENA |
REPOSITORIES: ENA
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Project description:To investigate whether lncRNAs are involved in intergenerational inheritance of obesity and obesity-induced decline in fertility, we divided mice into obesity (F0 mice fed a high-fat diet, F0-HFD) and non-obese (F0 mice fed normal chow, F0-NC) model groups and their male offspring (F1-HFD and F1-NC, respectively). We examined the differences in the expression levels of lncRNAs and mRNAs in the F0-HFD/F0-normal and F1-HFD/F1-normal groups. The results revealed similar expression patterns in the F1-HFD/F0-HFD groups at both the lncRNA and mRNA levels. The maximum difference in the lncRNA expression was observed between the F0-HFD and F0-NC groups. The differentially expressed lncRNA targets and mRNAs identified in our study are mainly involved in GnRH signalling pathway, metabolic process, and Hippo signalling pathway; similarly expressed lncRNAs and mRNAs in F1-HFD/F0-HFD are closely linked with G-protein coupled receptor signalling pathway, pancreatic polypeptide receptor activity, and lysine biosynthesis, which may play an important role in the molecular mechanism of intergenerational inheritance of obesity. Furthermore, potential genes that might play important roles in the pathogenesis of obesity-related low fertility were revealed by lncRNA-and mRNA-interaction studies based on the microarray expression profiles. In conclusion, we found that lncRNA could be involved in obesity-induced infertility by expressing abnormalities, which could act as genetic vectors of paternal inheritance of obesity.
2018-08-03 | GSE118039 | GEO
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: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
2013-02-14 | GSE44301 | GEO
Project description:Long non-coding RNAs (lncRNAs) play an important role in epigenetic regulation, and abnormalities may lead to male infertility. To investigate whether lncRNAs are involved in intergenerational inheritance of obesity and obesity-induced decline in fertility, we divided mice into obesity (F0 mice fed a high-fat diet, F0-HFD) and non-obese (F0 mice fed normal chow, F0-NC) model groups and their male offspring (F1-HFD and F1-NC, respectively). We examined the differences in the expression levels of lncRNAs and mRNAs in the F0-HFD/F0-NC and F1-HFD/F1-NC groups. The results revealed similar expression patterns in the F1-HFD/F0-HFD groups at both the lncRNA and mRNA levels. The maximum difference in the lncRNA expression was observed between the F0-HFD and F0-NC groups. The differentially expressed lncRNA targets and mRNAs identified in our study are mainly involved in GnRH signalling pathway, metabolic process, and Hippo signalling pathway; similarly expressed lncRNAs and mRNAs in F1-HFD/F0-HFD are closely linked with G-protein coupled receptor signalling pathway, pancreatic polypeptide receptor activity, and lysine biosynthesis, which may play an important role in the molecular mechanism of intergenerational inheritance of obesity. Furthermore, potential genes that might play important roles in the pathogenesis of obesity-related low fertility were revealed by lncRNA-and mRNA-interaction studies based on the microarray expression profiles. In conclusion, we found that lncRNA could be involved in obesity-induced infertility by expressing abnormalities, which could act as genetic vectors of paternal inheritance of obesity.
| S-EPMC5564612 | biostudies-literature
Project description:[This corrects the article DOI: 10.18632/oncotarget.18138.].
| S-EPMC6366817 | biostudies-literature
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:The paternal heredity of obesity and diabetes induced by a high-fat and/or high-sugar diet (Western-like diet) has been demonstrated through epidemiological analysis of human cohorts and experimental analysis, but the nature of the hereditary vector inducing this newly acquired phenotype is not yet well defined. Here, we show that microinjection of either testis or sperm RNA of male mice fed a Western-like diet into naive one-cell embryos leads to the establishment of the Western-like diet-induced metabolic phenotype in the resulting progenies, whereas RNAs prepared from healthy controls did not. Among multiple sequence differences between the testis transcriptomes of the sick and healthy fathers, we noted that several microRNAs had increased expression, which was of interest because this class of noncoding RNA is known to be involved in epigenetic control of gene expression. When microinjected into naive one-cell embryos, one of these small RNA, i.e., the microRNA miR19b, induced metabolic alterations that are similar to the diet-induced phenotype. Furthermore, this pathological phenotype was inherited by the offspring after crosses with healthy partners. Our results indicate that acquired food-induced trait inheritance might be enacted by RNA signalling.
| S-EPMC4677355 | biostudies-literature
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:Cellular telomere length is linked to replicative life span. Telomere repeats are lost in peripheral blood cells in vivo by age, and women show less telomere attrition than men. Previous reports have indicated that telomere length and chromosome-specific telomere-length patterns partly are inherited. The mode of heredity has not been clarified, but a link to the X chromosome was recently suggested. We analyzed peripheral mononuclear cells from 49 unrelated families for telomere length using a real-time PCR method. Short-term cultured Epstein-Barr virus-transformed lymphoblasts from the same individuals (n = 130) were analyzed for ability to maintain telomere length and possible gender-linked inheritance. A statistically significant association between telomere lengths comparing father-son (P = 0.011, n = 20) and father-daughter (P = 0.005, n = 22) pairs was found. However, no correlation was observed between mother-daughter (P = 0.463, n = 23) or mother-son (P = 0.577, n = 18). The father-offspring correlation was highly significant (P < 0.0001), in contrast to mother-offspring (P = 0.361). Epstein-Barr virus cultures demonstrated in most cases telomere preservation inversely related to initial mononuclear cell telomere length with short telomeres displaying the most pronounced elongation. Telomere length is inherited, and evidence for a father-to-offspring heritage of this trait was obtained, whereas in vitro telomere length maintenance was found to be dependent on the initial telomere length.
| S-EPMC1283414 | biostudies-literature