High sugar but not high fat diet consumption induces hepatic metabolic disruption and up-regulation of mitochondrial fission-associated protein Drp1 in a model of moderate obesity

Identification of new modifications and the association with diet patterns are essential for the prevention of non-alcoholic fatty liver disease (NAFLD). To address this problem, we feed rats with high caloric diets based on high sucrose (HSD) and high fat (HFD) and analysed metabolic and mitochondr...

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Published in:Archives of physiology and biochemistry 2023-01, Vol.129 (1), p.233-240
Main Authors: Cruz Hernández, Jarumi Hishel, Rosado Lomán, Wendy Natalia, Gómez-Crisóstomo, Nancy Patricia, De la Cruz-Hernández, Erick Natividad, Guzmán García, Luz María, Gómez Gómez, Montserrat, Hernández del Ángel, Nadia Arely, Aguilar Gamas, Carlos Francisco, Cruz Hernández, Vania Sherel, Martinez-Abundis, Eduardo
Format: Article
Language:English
Subjects:
Animals
Diet, High-Fat - adverse effects
energetic metabolism
Liver - metabolism
liver steatosis
Mitochondrial Dynamics
Non-alcoholic Fatty Liver Disease - pathology
Obesity
Obesity - metabolism
oxidative stress
PPAR gamma - metabolism
Rats
Sucrose - metabolism
Sugars - metabolism
Up-Regulation
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Summary:Identification of new modifications and the association with diet patterns are essential for the prevention of non-alcoholic fatty liver disease (NAFLD). To address this problem, we feed rats with high caloric diets based on high sucrose (HSD) and high fat (HFD) and analysed metabolic and mitochondrial alterations. Both diets induce moderated obesity and fat accumulation in the liver after 8, 10 and 12 months of diet. The HSD induces both hyperleptinemia and hyperinsulinemia, as well as up-regulation of transcription factors SRBEP1 and PPARγ along slight increase nitrosylation of proteins and increased mitochondrial fission. In contrast, HFD induced hyperleptinemia without changes in neither insulin levels nor oxidative stress, SREBP1, PPARγ, or mitochondrial dynamics. In conclusion, chronic consumption of high sucrose content diets induces more pathological and metabolic alteration in liver in comparison with consumption of high-fat content diets, although both induces obesity and liver steatosis in these animal models.
ISSN:1381-3455
1744-4160
DOI:10.1080/13813455.2020.1812666