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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
DJ-1 Deficiency Protects Hepatic Steatosis by Enhancing Fatty Acid Oxidation in Mice
Min Xu1, Hailong Wu2, Meng Li1
1Department of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Abstract:
Our previous studies have shown that DJ-1 play important roles in progression of liver diseases through modulating hepatic ROS production and immune response, but its role in hepatic steatosis remains obscure. In the present study, by adopting a high-fat-diet (HFD) induced mice model, we found that DJ-1 knockout (DJ-1 ) mice showing decreased HFD-induced obesity and visceral adipose accumulation. In line with these changes, there were also reduced liver weight and ameliorated hepatic triglyceride (TG) accumulation in DJ-1-/- mice compared to wild-type (WT) mice. And there were also decreased blood glucose levels and insulin resistance and reduced glucose metabolic disorder in DJ-1-/- mice, whereas there were no significant differences in total cholesterol (TC) and serum lipid in two groups of mice. Mechanistically, we found that there were no differences in food intake in these two genotypes of mice. Furthermore, there were no significant differences in fatty acid synthesis and glycolysis, but the expression of key enzymes in fatty acid oxidation and the tricarboxylic acid (TCA) cycle, such as Cpt1α, Pparα, Acox1, Cs, Idh1 and Idh2, was increased in DJ-1-/- mice liver, suggesting that there was enhanced fatty acids oxidation and TCA cycle in DJ-1-/- mice. Our data indicate that deletion of DJ-1 enhancing fatty acids oxidation resulting in lower hepatic TG accumulation in mice, which protecting mice hepatic steatosis.
Insights
Deleting DJ-1 protein reduces obesity and liver fat accumulation in mice by boosting fatty acid oxidation. This finding offers new insights into protecting against hepatic steatosis.
Area of Science:
- Biochemistry
- Metabolic diseases
- Molecular biology
Background:
- DJ-1 protein's role in liver disease progression is known, but its specific function in hepatic steatosis is unclear.
- Previous research indicates DJ-1 influences hepatic reactive oxygen species (ROS) production and immune responses.
Purpose of the Study:
- To investigate the role of DJ-1 in high-fat diet (HFD)-induced hepatic steatosis.
- To elucidate the molecular mechanisms by which DJ-1 affects fat metabolism in the liver.
Main Methods:
- Utilized a high-fat diet (HFD) induced mouse model.
- Compared DJ-1 knockout (DJ-1-/-) mice with wild-type (WT) mice.
- Analyzed metabolic parameters, liver weight, hepatic triglyceride (TG) content, blood glucose, insulin resistance, and gene/enzyme expression related to fatty acid metabolism and the TCA cycle.
Main Results:
- DJ-1 knockout mice exhibited reduced HFD-induced obesity, visceral adipose tissue accumulation, liver weight, and hepatic TG content compared to WT mice.
- DJ-1-/- mice showed improved glucose metabolism, decreased blood glucose levels, and reduced insulin resistance.
- Enhanced expression of key enzymes involved in fatty acid oxidation and the tricarboxylic acid (TCA) cycle was observed in DJ-1-/- mice livers, indicating increased metabolic activity.
Conclusions:
- Deletion of DJ-1 enhances fatty acid oxidation and TCA cycle activity.
- This enhanced metabolism leads to reduced hepatic triglyceride accumulation and protects against hepatic steatosis in mice.
- DJ-1 deficiency ameliorates metabolic disorders associated with high-fat diets.
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