The offspring from rats fed a fatty diet display impairments in the activation of liver peroxisome proliferator activated receptor alpha and features of fatty liver disease.

Maternal obesity programs liver derangements similar to those of NAFLD. Our main goal was to evaluate whether these liver anomalies were related to aberrant PPARα function. Obesity was induced in female Albino-Wistar rats by a fatty diet (FD rats). Several parameters related to NAFLD were evaluated in both plasma and livers from fetuses of 21 days of gestation and 140-day-old offspring. FD fetuses and offspring developed increased levels of AST and ALT, signs of inflammation and oxidative and nitrative stress-related damage. FD offspring showed dysregulation of Plin2, CD36, Cyp4A, Aco, Cpt-1, Hadha and Acaa2 mRNA levels, genes involved in lipid metabolism and no catabolic effect of the PPARα agonist clofibrate. These results suggest that the FD offspring is prone to develop fatty liver, a susceptibility that can be linked to PPARα dysfunction, and that this could in turn be related to the liver impairments programmed by maternal obesity.

• Publication year

  2020

• Venue

  Molecular and Cellular Endocrinology

• Publication date

  2020-04-13

• Fields of study

  Biology, Medicine, Environmental Science

• Identifiers
  DOI 10.1016/j.mce.2020.110818PMID 32298755
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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