RESEARCH Molecular hydrogen atten 2

Full list of author information is available at the end of the articlelems. There is accumulating evidence that obesity is closely associated with impaired free fatty acid (FFA) metabolism as well as insulin resistance and inflamma-tion [1]. Excessive release of FFA from visceral fat adipo-cytes leads to the production of inflammatory and proatherogenic proteins through activation of the NFκB and c-Jun NH2-terminal kinase (JNK) pathways in chain fatty acids in diverse cell types such as monocytes, platelets, macrophages, microvascular endothelial cells, adipocytes, muscle cells, enterocytes, and hepatocytes [2]. Mice deficient of CD36 exhibit defective uptake and utilization of fatty acids. Excessive fatty acid uptake me-diated by CD36 plays an important role in hepatic steatosis [3]. The expression level of CD36 is very low in normal liver tissues [4], but is drastically increased in the liver tissues of high-fat diet (HFD)-induced fatty liver mice and those of human NAFLD. Conversely, forced expression of CD36 in liver causes hepatic steatosis in * Correspondence