Zac1 and the Imprinted Gene Network program juvenile NAFLD in response to maternal metabolic syndrome.

ABSTRACT:

Background and aims

Within the next decade, NAFLD is predicted to become the most prevalent cause of childhood liver failure in developed countries. Predisposition to juvenile NAFLD can be programmed during early life in response to maternal metabolic syndrome (MetS), but the underlying mechanisms are poorly understood. We hypothesized that imprinted genes, defined by expression from a single parental allele, play a key role in maternal MetS-induced NAFLD, due to their susceptibility to environmental stressors and their functions in liver homeostasis. We aimed to test this hypothesis and determine the critical periods of susceptibility to maternal MetS.

Approach and results

We established a mouse model to compare the effects of MetS during prenatal and postnatal development

SUBMITTER: Baptissart M 

PROVIDER: S-EPMC9314464 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature