Adelheid Soubry

TL;DR: The data indicate a preconceptional impact of paternal obesity on the reprogramming of imprint marks during spermatogenesis and suggest an increase in DNA methylation at the IGF2 and H19 DMRs among newborns from obese mothers, but a larger study is warranted to further explore the potential effects of maternal obesity or lifestyle on the offspring's epigenome.

TL;DR: A significant and independent association between paternal obesity and the offspring’s methylation status suggests the susceptibility of the developing sperm for environmental insults and altered methylation outcomes at multiple imprint regulatory regions in children born to obese parents, compared with childrenBorn to non-obese parents.

TL;DR: This essay suggests the existence of epigenetic windows of susceptibility to environmental insults during sperm development and suggests changes in DNA methylation, histone modification, and non‐coding RNAs are viable mechanistic candidates for a non‐genetic transfer of paternal environmental information, from maturing germ cell to zygote.

TL;DR: The data support that male overweight/obesity status is traceable in the sperm epigenome, and set the groundwork for future studies investigating male gametic methylation aberrations due to paternal lifestyle factors such as obesity.

TL;DR: In this paper, the authors combined data from 14 U.S. epidemiologic studies for which their laboratory group previously assessed exposure to two commonly used organophosphate compounds, tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and triphenyl phosphate (TPHP).