Male obesity could damage future children’s metabolic health through epigenetic factors carried in sperm, a study showed, indicating the importance of paternal health before conception.
The study, titled “Male obesity causes adipose mitochondrial dysfunction in F1 mouse progeny via a let-7-DICER axis” and conducted by a research team led by Huang Chien (黃謙), an assistant professor at National Taiwan University’s (NTU) Department of Animal Science and Technology, was published in the journal Nature Communications on Feb. 24.
According to the WHO, more than 1 billion people globally are classified as obese. As the global obesity population grows, scientists have increasingly focused on how parental environments influence the health of offspring, NTU said in a press release on Wednesday.
Photo: Screen grab from National Taiwan University’s Web site
While previous studies largely examined the effects of maternal physiological conditions on embryonic development, whether paternal health traits can be “inherited” by the next generation has become a research focus in the past few years, NTU said.
Huang’s team has proved for the first time that paternal obesity can affect offspring metabolism and adipose tissue health through epigenetic factors in sperm, the university said.
The researchers found that obesity and weight loss in male mice reversibly alter metabolism and impair adipose mitochondrial function, and that these metabolic aberrations are transmitted to male offspring, which display reduced mitochondrial gene expression.
The researchers identified microRNAs let-7d/e as epigenetic mediators induced in sperm of the obese male mice, and in their adipose tissue and that of their male offspring, where the molecules silence the miRNA processor DICER1 and impair mitochondrial activity, the study showed.
Researchers microinjected let-7d/e into healthy embryos and found glucose intolerance and mitochondrial gene suppression in sired offspring, they said.
Single-cell RNA sequencing of blastomeres reveals that let-7d/e impair oxidative metabolism in early embryos, they added.
Lifestyle-induced weight loss in males with obesity downregulates human HSA-LET-7D/E in semen, indicating a conserved role for let-7 in transmission of metabolic health, they said.
The findings demonstrate that microRNA let-7 in sperm reprograms offspring metabolism by modulating mitochondrial function during early development, they said.
The study not only overturns traditional perceptions of inheritance, but also proves that acquired environmental factors such as diet and weight can write a “metabolic memory” into the epigenetic code of sperm, NTU said.
The findings reveal that the molecular mechanisms by which paternal obesity affects the metabolic health of offspring, offering a new research direction for the transgenerational prevention and treatment of metabolic syndrome, it said.
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