Paternal high-fat diet altered sperm 5'tsRNA-Gly-GCC is associated with enhanced gluconeogenesis in the offspring
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA807657 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18052100.fastq.gz | Fastqsanger.gz | |||
| SRR18052091.fastq.gz | Fastqsanger.gz | |||
| SRR18052092.fastq.gz | Fastqsanger.gz | |||
| SRR18052093.fastq.gz | Fastqsanger.gz | |||
| SRR18052094.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we aimed to find out how the sperm tsRNA involved in paternal high-fat diet induced abnormal gluconeogenesis of F1 offspring, and explore the underlying molecular mechanism of its regulation.
2022-02-18 | GSE196881 | GEO
Project description:Background: Paternal lifestyle, stress and environmental exposures play a crucial role in the health of offspring and are associated with non-genetic inheritance of acquired traits, however the underlying mechanisms are unclear. In this study, we aimed to find out how the sperm tsRNA involved in paternal high-fat diet induced abnormal gluconeogenesis of F1 offspring, and explore the underlying molecular mechanism of its regulation. Method: We generated a paternal high fat diet (42% kcal fat) model to investigate the mechanism by which paternal diet affects offspring metabolism. Four-week-old C57BL/6J male mice were randomly assigned into two groups to receive either a control diet (CD; 10% kcal fat) or a high-fat (HFD; 42% kcal fat) diet for 10 weeks, and mice from each group were then mated with 8-week-old females with control diet in a 1:2 ratio to generate F1. F0 sperms were isolated and small RNAs was sequenced by high-throughput sequencing. Metabolic phenotypes were examined with both F0 and F1. Results: A significant increase in body weight was observed with HFD-F0 mice at 8 weeks of age as compared to CD mice at the same age. F0 mice showed impaired glucose tolerance (GTT), resistance to insulin tolerance (ITT) and increased pyruvate tolerance (PTT) at 14 weeks. HFD-F1 male mice showed no significant difference in body weight. An increase in PTT was found at 13 weeks of age and no significant changes in GTT and ITT. PEPCK and G6Pase that related to gluconeogenesis increased significantly in the liver of HFD-F1 male mice. Sperm sequencing results showed that 5'tsRNA-Gly-GCC derived from tRNA-Gly-GCC-2 specifically was remarkably upregulated in sperm of HFD F0 mice. Q-PCR further showed that this tsRNA was also increased in the liver of HFD-F1 comparison with CD-F1 mice. In addition, we found that 5'tsRNA-Gly-GCC can regulate Sirt6-FoxO1 pathway and be involved in the gluconeogenesis pathway in liver. Conclusion: 5'tsRNA-Gly-GCC that increased in HFD mice mature sperms can promote gluconeogenesis in liver by regulating Sirt6-FoxO1 pathway, which might represent a potential paternal epigenetic factor mediating the intergenerational inheritance of diet-induced metabolic alteration.
| S-EPMC9035875 | biostudies-literature
Project description:Breast cancer (BC) is a leading cause of female mortality worldwide, largely due to metastatic progression and the absence of reliable non-invasive biomarkers for early detection. This study investigates the potential of tRNA-derived small RNA fragments (tRFs) as novel diagnostic and functional molecules in BC. Through high-throughput sequencing and subsequent validation in clinical cohorts, we identified tsRNA-Gly-5-0006 as significantly downregulated in both BC tissues and patient serum compared to adjacent normal tissues, mastitis samples, and healthy controls.
2026-02-14 | GSE319387 | GEO
Project description:Acute coronary syndrome (ACS) is one of the leading causes of death worldwide. Aberrant expression of Transfer RNA-derived small RNAs (tsRNA) contributed to various human disease. However, the clincal utility and biological function of tsRNA in ACS are largely unknown. High throughput sequencing revealed a landscape of novel sncRNAs in the human PBMCs. tsRNAs represented a characteristic expression pattern in responding to acute coronary syndrome; tRF-Gly-GCC-06 and tRF-Lys-CTT-02 were significantly up-regulated in patients with unstable angina(UA) and acute myocardial infarction(AMI). Both of the two tRFs demonstrated reasonable diagnostic accuracy for ACS detection. tRF-Gly-GCC-06 and tRF-Lys-CTT-02 upregulation were independent predictors of an increased risk of ACS. Both of the two tRFs expression levels show a significantly positive correlation with Gensini score.Our study identified novel tsRNA alterations associated with ACS and provided potential clinical biomarkers and therapeutic targets.
2025-04-30 | GSE279975 | GEO
Project description:Acute coronary syndrome (ACS) is one of the leading causes of death worldwide. Aberrant expression of Transfer RNA-derived small RNAs (tsRNA) contributed to various human disease. However, the clincal utility and biological function of tsRNA in ACS are largely unknown. High throughput sequencing revealed a landscape of novel sncRNAs in the human PBMCs. tsRNAs represented a characteristic expression pattern in responding to acute coronary syndrome; tRF-Gly-GCC-06 and tRF-Lys-CTT-02 were significantly up-regulated in patients with unstable angina(UA) and acute myocardial infarction(AMI). Both of the two tRFs demonstrated reasonable diagnostic accuracy for ACS detection. tRF-Gly-GCC-06 and tRF-Lys-CTT-02 upregulation were independent predictors of an increased risk of ACS. Both of the two tRFs expression levels show a significantly positive correlation with Gensini score.Our study identified novel tsRNA alterations associated with ACS and provided potential clinical biomarkers and therapeutic targets.
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Project description:Serum tsRNA-Gly-5-0006 in breast cancer: Differential expression and effects on cancer cell biology
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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 unexplored. 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 birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>
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Project description:Cells were grown to early log phase (OD600 ~ 0.2) at 30oC in 1 liter of minimal B medium (Cherest, H., and Surdin-Kerjan, Y. (1992) Genetics 130, 51-58) with or without supplementation with 10 mM glycine and harvested. All cells were harvested by rapid centrifugation at room temperature then flash frozen in liquid nitrogen. Arrays compared expression of Gly- cells to the Gly+ controls. Strain BY4741 was the wild type and several deletion strains were also used. Keywords: parallel sample
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Project description:Paternal nicotine exposure can alter phenotypes in future generations. To explore whether paternal nicotine exposure affects the hepatic repair to chronic injury which would lead to hepatic fibrosis in offspring, we establish a paternal effect model based on nicotine exposure in mice.
2020-07-31 | GSE155308 | GEO
Project description:Cells were grown to early log phase (OD600 ~ 0.2) at 30oC in 1 liter of minimal B medium (Cherest, H., and Surdin-Kerjan, Y. (1992) Genetics 130, 51-58) with or without supplementation with 10 mM glycine and harvested. All cells were harvested by rapid centrifugation at room temperature then flash frozen in liquid nitrogen. Arrays compared expression of Gly- cells to the Gly+ controls. Strain BY4741 was the wild type and several deletion strains were also used. Keywords: parallel sample
2004-07-17 | E-GEOD-1553 | biostudies-arrayexpress