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Review highlights epigenetic transmission and developmental programming affecting obesity and type 2 diabetes risk.
Type 2 diabetes, which is closely linked to obesity, results from complex genetic and environmental interactions. Despite high heritability estimates, genome-wide association studies have not fully explained the heritability, suggesting the involvement of epigenetic mechanisms. This review highlights two distinct genome-independent pathways for intergenerational transmission of diabetic risk: (1) epigenetic transmission via gametes, whereby parental exposures induce heritable epigenetic changes in germ cells, and (2) developmental programming, in which prenatal or early postnatal environments shape the metabolism of offspring. Both processes are increasingly understood to involve epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNAs. These epigenetic modifications have been suggested to contribute to intergenerational disease transmission in both animal and human studies. Understanding these mechanisms is essential for developing preventive strategies targeting the intergenerational risk of metabolic diseases.
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Chisayo Kozuka (2025) studied this question.
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