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
| Autor: | Verónica White, María Belén Mazzucco, Sabrina Lorena Roberti, Daiana Fornes, Florencia Heinecke, Alicia Jawerbaum |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Offspring CD36 030209 endocrinology & metabolism Inflammation Diet High-Fat Biochemistry 03 medical and health sciences 0302 clinical medicine Endocrinology Fetus Non-alcoholic Fatty Liver Disease Internal medicine medicine Animals PPAR alpha Clofibrate RNA Messenger Rats Wistar Molecular Biology biology business.industry Fatty liver Lipid metabolism medicine.disease Lipid Metabolism 030104 developmental biology Gene Expression Regulation Liver biology.protein Female Peroxisome proliferator-activated receptor alpha medicine.symptom business medicine.drug |
| Zdroj: | Molecular and cellular endocrinology. 511 |
| ISSN: | 1872-8057 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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