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Background And Aims: Maternal obesity increases the risk of the paediatric form of metabolic dysfunction-associated steatotic liver disease (MASLD), affecting up to 30% of youth, but the developmental origins remain poorly understood.

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A Guinea Pig Model of Pediatric Metabolic Dysfunction-Associated Steatohepatitis: Poor Vitamin C Status May Advance Disease.

Nutrients

January 2025

Section of Preclinical Disease Biology, Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 1870 Frederiksberg, Denmark.

Children and teenagers display a distinct metabolic dysfunction-associated steatohepatitis (MASH) phenotype, yet studies of childhood MASH are scarce and validated animal models lacking, limiting the development of treatments. Poor vitamin C (VitC) status may affect MASH progression and often co-occurs with high-fat diets and related metabolic imbalances. As a regulator of DNA methylation, poor VitC status may further contribute to MASH by regulating gene expression This study investigated guinea pigs-a species that, like humans, depends on vitC in the diet-as a model of pediatric MASH, examining the effects of poor VitC status on MASH hallmarks and global DNA methylation levels.

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Hepatic encephalopathy (HE) in dogs is a metabolic disorder of the central nervous system that occurs secondarily to liver dysfunctions, whether due to acquired or congenital causes. A portosystemic shunt is the presence of abnormal communications between the hepatic vessels (portal and suprahepatic veins). As a result of this, the blood brought from the digestive tract through the portal vein bypasses the liver, and the unmetabolized components of the portal bloodstream enter directly into systemic circulation, causing clinical symptoms of metabolic encephalopathy (HE).

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