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

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
• liver steatosis
• oxidative stress
• mitochondrial dynamics
• energetic metabolism

Acknowledgements

The authors are grateful to Fernanda Hernández Landero for her technical assistance.

The authors wish to dedicate this work to the memory of their colleague and friend Teresa Ramón Frias, who support the development of research in their Division.

Disclosure statement

The authors declare that there are no conflicts of interest.

Data availability statement

The data that support the findings of this study are available from the corresponding author, [EM-A], upon reasonable request.

Additional information

Funding

This research was partially supported by the National Council of Science and Technology [CONACYT, grants 2015–257849 to NPGC and 2013–222290-M to EMA].