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Comment
. 2018 Jan;67(1):7-9.
doi: 10.1002/hep.29416. Epub 2017 Nov 13.

Perinatal programming of adolescent nonalcoholic fatty liver disease: A case for gender inequality?

Monika Sarkar  1 , Gyorgy Baffy  2
Affiliations
Comment

Perinatal programming of adolescent nonalcoholic fatty liver disease: A case for gender inequality?

Monika Sarkar et al. Hepatology. 2018 Jan.
No abstract available

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Conflict of interest statement

Potential conflict of interest: Nothing to report.

Figures

FIG. 1
FIG. 1
Perinatal programming and sexual dimorphism in the development of adolescent NAFLD. Major periods of early life and potential mechanisms of metabolic vulnerabilities leading to NAFLD are illustrated schematically. The offspring genome assembled at conception includes genetic variance (e.g., single nucleotide polymorphism) and nongenetic effects of parental life experiences via gamete imprinting that may drive future susceptibility to disease. Gene expression and function is further modified by environmental effects during gestation and in postnatal life with a heritable impact (epigenetic modifications) or with changes limited to the individual’s lifetime. The work of Ayonrinde et al.(3) indicates that adolescent NAFLD is associated with parental factors in the preconception period (e.g., paternal and maternal obesity), in utero (e.g., gestational weight gain), and in early postnatal life (e.g., breastfeeding linked to socioeconomic status). The “baggage” of developmental programming carried through the life of offspring shows remarkable sexual dimorphism and includes different characteristics linked to adolescent NAFLD among girls and boys. Additional postnatal insults (e.g., obesogens) and comorbidities (e.g., obesity and diabetes) may further modify the risk of NAFLD in offspring and subsequent progeny with potential escalation of the liver disease phenotype.
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