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Differences in Fatty Acid Metabolism between MCDD and HFD Induced Metabolic Dysfunction-associated Fatty Liver
Jia-Xuan Wang1,2, Xin-Zhu Liu3,4, Zhen Guo1,5
1Institute of Interdisciplinary Science, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Background:
The global incidence of metabolic dysfunction-associated fatty liver disease (MAFLD) is increasing annually, which has become a major public-health concern. MAFLD is typically associated with obesity, hyperlipemia, or metabolic syndrome. Dietary induction is one of the most common methods for preparing animal models of MAFLD. However, there are phenotypic differences between methionine-choline-deficient diet (MCDD) and high fat diet (HFD) models.
Methods:
To explore the differences in hepatic fatty acid metabolism between MCDD and HFD induced MAFLD, we analyzed serum and liver tissue from the two MAFLD models.
Results:
We found that liver fat accumulation and liver function damage were common pathological features in both MAFLD models. Furthermore, in the MCDD model, the expression of hepatic fatty acid transport proteins increased, while the expression of hepatic fatty acid efflux proteins and mRNA decreased, along with a decrease in blood lipid levels. In the HFD model, the expression of hepatic fatty acid uptake proteins, efflux proteins and efflux mRNA increased, along with an increase in blood lipid levels.
Conclusion:
Impaired fatty acid oxidation and increased hepatic fatty acid uptake play key roles in the pathogenesis of the two MAFLD models. The inverse changes in de novo lipogenesis and fatty acid efflux may represent an important pathological mechanism that leads to the phenotypic differences between the MCDD and HFD models.
Insights
Metabolic dysfunction-associated fatty liver disease (MAFLD) models induced by methionine-choline-deficient diet (MCDD) and high-fat diet (HFD) show distinct hepatic fatty acid metabolism changes. These differences are crucial for understanding MAFLD pathogenesis.
Area of Science:
- Hepatology
- Metabolic Diseases
- Animal Models
Background:
- Metabolic dysfunction-associated fatty liver disease (MAFLD) incidence is rising globally, posing a significant public health challenge.
- MAFLD is commonly linked to obesity, hyperlipemia, and metabolic syndrome.
- Dietary induction is a primary method for creating MAFLD animal models, with notable phenotypic variations between methionine-choline-deficient diet (MCDD) and high-fat diet (HFD) models.
Purpose of the Study:
- To investigate the distinct hepatic fatty acid metabolic pathways in MCDD-induced versus HFD-induced MAFLD models.
- To elucidate the molecular mechanisms underlying phenotypic differences in these MAFLD models.
Main Methods:
- Analysis of serum and liver tissue from established MCDD and HFD induced MAFLD animal models.
- Comparative assessment of hepatic fatty acid transport, uptake, and efflux protein and mRNA expression.
Main Results:
- Both MCDD and HFD models exhibited liver fat accumulation and functional damage.
- MCDD model showed increased fatty acid transport protein expression, decreased efflux protein/mRNA, and lower blood lipids.
- HFD model demonstrated increased fatty acid uptake, efflux protein, and efflux mRNA expression, alongside elevated blood lipids.
Conclusions:
- Impaired fatty acid oxidation and enhanced hepatic fatty acid uptake are central to both MAFLD models.
- Divergent regulation of de novo lipogenesis and fatty acid efflux contributes to the phenotypic disparities between MCDD and HFD models.
