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Obesity linked to sperm health, potentially affecting offspring metabolism

From Liberty Times · () Chinese

Translated from Chinese, summarized and contextualized by DistantNews.

At a glance

News Named sources Outcome reported
  • A new study from National Taiwan University suggests that paternal obesity can negatively impact offspring's metabolic health through epigenetic factors in sperm.
  • Researchers found that obesity in male mice reversibly alters metabolism and impairs adipose mitochondrial function, with these effects transmitted to male offspring.
  • The study identified microRNAs let-7d/e as key epigenetic mediators, demonstrating that acquired environmental factors like weight can influence future generations' health.

Paternal obesity may damage future children's metabolic health through epigenetic factors carried in sperm, according to a study from National Taiwan University (NTU). The research highlights the critical importance of paternal health before conception.

Male obesity causes adipose mitochondrial dysfunction in F1 mouse progeny via a let-7-DICER axis

— Study TitleThe title of the research published in Nature Communications.

The study, published in Nature Communications, was led by Huang Chien, an assistant professor at NTU's Department of Animal Science and Technology. It provides the first proof that paternal obesity can affect offspring metabolism and adipose tissue health via epigenetic factors in sperm. This challenges traditional perceptions of inheritance and shows acquired environmental factors can create a "metabolic memory" in sperm.

Researchers observed that obesity and subsequent weight loss in male mice reversibly altered metabolism and impaired adipose mitochondrial function. These metabolic aberrations were transmitted to their male offspring, who exhibited reduced mitochondrial gene expression. The study identified specific microRNAs, let-7d/e, as epigenetic mediators induced in the sperm of obese male mice and present in their offspring's adipose tissue.

paternal obesity can affect offspring metabolism and adipose tissue health through epigenetic factors in sperm

— National Taiwan UniversityDescribing the key finding of the study.

These microRNAs silence the miRNA processor DICER1, impairing mitochondrial activity. When microinjected into healthy embryos, let-7d/e caused glucose intolerance and mitochondrial gene suppression in the resulting offspring. The findings demonstrate that microRNAs in sperm can reprogram offspring metabolism by modulating mitochondrial function during early development, underscoring the role of lifestyle in intergenerational health.

acquired environmental factors such as diet and weight can write a “metabolic memory” into the epigenetic code of sperm

— National Taiwan UniversityExplaining the broader implications of the research.
DistantNews Editorial

Originally published by Liberty Times in Chinese. Translated, summarized, and contextualized by our editorial team with added local perspective. Read our editorial standards.

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