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

Arch Physiol Biochem. 2023 Feb;129(1):233-240. doi: 10.1080/13813455.2020.1812666. Epub 2020 Sep 3.

Abstract

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.

Keywords: Obesity; energetic metabolism; liver steatosis; mitochondrial dynamics; oxidative stress.

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects
  • Liver / metabolism
  • Mitochondrial Dynamics*
  • Non-alcoholic Fatty Liver Disease* / pathology
  • Obesity / metabolism
  • PPAR gamma / metabolism
  • Rats
  • Sucrose / metabolism
  • Sugars / metabolism
  • Up-Regulation

Substances

  • PPAR gamma
  • Sucrose
  • Sugars
  • Dnm1l protein, rat