Research reveals that a father's high-fat diet can influence offspring's metabolic health through changes in sperm mitochondrial RNA, potentially leading to glucose intolerance.
By Vijay Kumar MalesuJun 7 2024Reviewed by Susha Cheriyedath, M.Sc. In a recent review published in the journal Nature, a group of researchers investigated how preconception high-fat diet affects epididymal spermatozoa and the role of mitochondrial transfer Ribonucleic Acid in influencing offspring metabolic health.
Epididymal sperm susceptibility to diet To investigate how epididymal spermatozoa respond to environmental influences and to discern the contributions of epididymal and spermatogenic information to paternal intergenerational effects, the team conducted an experiment on 6-week-old male mice. These mice were fed either an HFD or a low-fat diet for 2 weeks. After this dietary challenge, some of the treated males were mated directly to unexposed females to generate the F1 generation group).
Transcriptional signatures in offspring The differences in glucose tolerance between HFD-tolerant and HFD-intolerant offspring were associated with unique transcriptional signatures in metabolically relevant tissues. About 30% of the genes differentially expressed in HFDi mice were also linked to childhood obesity in humans. These genes are clustered into pathways related to mitochondrial function and inflammation.
Human studies on mt-tsRNAs In a study involving young Finnish volunteers, mt-tsRNAs were found to be positively associated with BMI. Although obtained from a small cohort, the findings suggest that mt-sncRNAs play important roles in responding to metabolic challenges in mice and humans.
Conception Diet Embryonic Development Fertilization Genes Genetic Glucose Obesity Research Ribonucleic Acid Sperm Transcription
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