Symposium 19: Paternal diabetes and epigenetic changes in sperm

Abstract

The interest in the possibility that the environmental exposure of epigenome of germinal cells, such as methylation of DNA, post-traductional modification of histones and/or small non-coding RNAs can be transferred to the next generations affecting its metabolic health has increased in the lasts years¹.

Until recently, most of the research has focused mainly in the study of programming due to the maternal exposition to an adverse environment or pathology. However, the programming of type 2 diabetes and obesity due to paternal programming has been evidenced in humans, a paradigm called “Paternal Origins of Health and Disease” (POHAD) that arises from the more known “Developmental Origins of Health and Disease” (DOHAD)². Studies of the paternal transmission have evidenced the influence of environment on epigenetic modifications in the germ cell line of males, leading to intergenerational and transgenerational phenotypes. The intergenerational effects in the offspring occurs when the father germ cells are directly affected from fetal life to adulthood whereas the transgenerational effects occur in absence of the exposition of father germ cells to the insult³.