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Itaconic acid underpins hepatocyte lipid metabolism in non-alcoholic fatty liver disease in male mice
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Itaconic acid underpins hepatocyte lipid metabolism in non-alcoholic fatty liver disease in male mice
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Journal Article
Itaconic acid underpins hepatocyte lipid metabolism in non-alcoholic fatty liver disease in male mice
2023
Overview
Itaconate, the product of the decarboxylation of
cis
-aconitate, regulates numerous biological processes. We and others have revealed itaconate as a regulator of fatty acid β-oxidation, generation of mitochondrial reactive oxygen species and the metabolic interplay between resident macrophages and tumors. In the present study, we show that itaconic acid is upregulated in human non-alcoholic steatohepatitis and a mouse model of non-alcoholic fatty liver disease. Male mice deficient in the gene responsible for itaconate production (immunoresponsive gene (Irg)-1) have exacerbated lipid accumulation in the liver, glucose and insulin intolerance and mesenteric fat deposition. Treatment of mice with the itaconate derivative, 4-octyl itaconate, reverses dyslipidemia associated with high-fat diet feeding. Mechanistically, itaconate treatment of primary hepatocytes reduces lipid accumulation and increases their oxidative phosphorylation in a manner dependent upon fatty acid oxidation. We propose a model whereby macrophage-derived itaconate acts in
trans
upon hepatocytes to modulate the liver’s ability to metabolize fatty acids.
In this study, Weiss, Palmieri et al. show that macrophage-derived itaconate impinges on hepatocyte lipid metabolism. This mechanism participates in the crosstalk of the immune system with hepatocytes during the development of non-alcoholic fatty liver disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
