Aberrant DNA Methylation Mediates the Transgenerational Risk of Metabolic and Chronic Disease Due to Maternal Obesity and Overnutrition.
Yan LiCarol A PollockSonia SaadPublished in: Genes (2021)
Maternal obesity is a rapidly evolving universal epidemic leading to acute and long-term medical and obstetric health issues, including increased maternal risks of gestational diabetes, hypertension and pre-eclampsia, and the future risks for offspring's predisposition to metabolic diseases. Epigenetic modification, in particular DNA methylation, represents a mechanism whereby environmental effects impact on the phenotypic expression of human disease. Maternal obesity or overnutrition contributes to the alterations in DNA methylation during early life which, through fetal programming, can predispose the offspring to many metabolic and chronic diseases, such as non-alcoholic fatty liver disease, obesity, diabetes, and chronic kidney disease. This review aims to summarize findings from human and animal studies, which support the role of maternal obesity in fetal programing and the potential benefit of altering DNA methylation to limit maternal obesity related disease in the offspring.
Keyphrases
- dna methylation
- insulin resistance
- birth weight
- weight gain
- metabolic syndrome
- weight loss
- type diabetes
- high fat diet induced
- pregnancy outcomes
- high fat diet
- gene expression
- chronic kidney disease
- genome wide
- human health
- healthcare
- early life
- pregnant women
- cardiovascular disease
- skeletal muscle
- body mass index
- public health
- poor prognosis
- risk assessment
- climate change
- end stage renal disease
- hepatitis b virus
- long non coding rna
- gestational age
- mental health
- physical activity
- induced pluripotent stem cells
- peritoneal dialysis
- intensive care unit
- respiratory failure
- drug induced
- binding protein
- pluripotent stem cells