Paternal eNOS deficiency in mice affects glucose homeostasis and liver glycogen in male offspring without inheritance of eNOS deficiency itself.
Berthold HocherYong-Ping LuChristoph ReichetzederXiaoli ZhangOleg TsuprykovJan RahnenführerLi XieJian LiLiang HuBernhard K KrämerAhmed A HasanPublished in: Diabetologia (2022)
Our study suggests that paternal genetic defects such as eNOS deficiency may alter the epigenome of the sperm without transmission of the paternal genetic defect itself. In later life wild-type male offspring of +/- eNOS fathers developed increased fasting insulin and increased insulin after glucose load. These effects are associated with increased Gr and Pgc1a gene expression due to altered methylation of these genes.
Keyphrases
- genome wide
- nitric oxide synthase
- wild type
- dna methylation
- pi k akt
- gene expression
- endothelial cells
- blood glucose
- type diabetes
- high fat diet
- nitric oxide
- glycemic control
- copy number
- replacement therapy
- signaling pathway
- cell proliferation
- mitochondrial dna
- metabolic syndrome
- adipose tissue
- blood pressure
- transcription factor