Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs.

ABSTRACT: Maternal obesity has deleterious effects on the process of establishing oocyte DNA methylation; yet the underlying mechanisms remain unclear. Here, we found that maternal obesity disrupted the genomic methylation of oocytes using a high-fat diet (HFD) induced mouse model, at least a part of which was transmitted to the F2 oocytes and livers via females. We further examined the metabolome of serum and found that the serum concentration of melatonin was reduced. Exogenous melatonin treatment significantly reduced the hyper-methylation of HFD oocytes, and the increased expression of DNMT3a and DNMT1 in HFD oocytes was also decreased. These suggest that melatonin may play a key role in the disrupted genomic methylation in the oocytes of obese mice. To address how melatonin regulates the expres

SUBMITTER: Chao S 

PROVIDER: S-EPMC11623932 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature