Mitochondrial role in the neonatal predisposition to developing nonalcoholic fatty liver disease

The Journal of Clinical Investigation
Peter R Baker, Jacob E Friedman

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a global epidemic in obese children and adults, and the onset might have fetal origins. A growing body of evidence supports the role of developmental programming, whereby the maternal environment affects fetal and infant development, altering the risk profile for disease later in life. Human and nonhuman primate studies of maternal obesity demonstrate that risk factors for pediatric obesity and NAFLD begin in utero. The pathologic mechanisms for NAFLD are multifactorial but have centered on altered mitochondrial function/dysfunction that might precede insulin resistance. Compared with the adult liver, the fetal liver has fewer mitochondria, low activity of the fatty acid metabolic enzyme carnitine palmitoyl-CoA transferase-1, and little or no gluconeogenesis. Exposure to excess maternal fuels during fetal life uniquely alters hepatic fatty acid oxidation, tricarboxylic acid cycle activity, de novo lipogenesis, and mitochondrial health. These events promote increased oxidative stress and excess triglyceride storage, and, together with altered immune function and epigenetic changes, they prime the fetal liver for NAFLD and might drive the risk for nonalcoholic steatohepatitis in the nex...Continue Reading

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Citations

Feb 12, 2020·Gastroenterology·Mohammed EslamUNKNOWN International Consensus Panel
Mar 16, 2021·Frontiers in Medicine·Anna Pia Delli BoviPietro Vajro
May 15, 2021·Frontiers in Pediatrics·Serdar BekenMustafa Serteser
Jun 3, 2021·International Journal of Environmental Research and Public Health·Oriol JuanolaIsabel Gómez-Hurtado
Aug 17, 2021·Frontiers in Physiology·Nyasha Charity MukonowenzouKennedy Honey Erlwanger

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Methods Mentioned

BETA
NMR
histone acetylation
biopsy

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