| Literature DB >> 26669700 |
Ida Donkin1, Soetkin Versteyhe1, Lars R Ingerslev1, Kui Qian1, Mie Mechta1, Loa Nordkap2, Brynjulf Mortensen3, Emil Vincent R Appel1, Niels Jørgensen2, Viggo B Kristiansen4, Torben Hansen1, Christopher T Workman5, Juleen R Zierath6, Romain Barrès7.
Abstract
Obesity is a heritable disorder, with children of obese fathers at higher risk of developing obesity. Environmental factors epigenetically influence somatic tissues, but the contribution of these factors to the establishment of epigenetic patterns in human gametes is unknown. Here, we hypothesized that weight loss remodels the epigenetic signature of spermatozoa in human obesity. Comprehensive profiling of the epigenome of sperm from lean and obese men showed similar histone positioning, but small non-coding RNA expression and DNA methylation patterns were markedly different. In a separate cohort of morbidly obese men, surgery-induced weight loss was associated with a dramatic remodeling of sperm DNA methylation, notably at genetic locations implicated in the central control of appetite. Our data provide evidence that the epigenome of human spermatozoa dynamically changes under environmental pressure and offers insight into how obesity may propagate metabolic dysfunction to the next generation.Entities:
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Year: 2015 PMID： 26669700 DOI： 10.1016/j.cmet.2015.11.004
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287