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Open Access Research

Molecular hydrogen attenuates fatty acid uptake and lipid accumulation through downregulating CD36 expression in HepG2 cells

Akio Iio1, Mikako Ito2, Tomohiro Itoh3, Riyako Terazawa4, Yasunori Fujita5, Yoshinori Nozawa6, Ikuroh Ohsawa7, Kinji Ohno2 and Masafumi Ito5*

Author Affiliations

1 Department of Embryology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya-Cho, Kasugai, Aichi, 480-0392, Japan

2 Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan

3 Faculty of Agriculture, Kinki University, 3327-204 Nakamachi, Nara, Nara, 631-0052, Japan

4 Department of Urology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu, Gifu, 501-1193, Japan

5 Research Team for Mechanism of Aging, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi, Tokyo, 173-0015, Japan

6 Department of Food and Health, Tokai Gakuin University, 5-68 Naka-kirinocho, Kakamigahara, Gifu, 504-8511, Japan

7 Research Team for Functional Biogerontology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi, Tokyo, 173-0015, Japan

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Medical Gas Research 2013, 3:6  doi:10.1186/2045-9912-3-6

Published: 1 March 2013

Abstract

Background

There is accumulating evidence that obesity is closely associated with an impaired free fatty acid metabolism as well as with insulin resistance and inflammation. Excessive fatty acid uptake mediated by fatty acid translocase CD36 plays an important role in hepatic steatosis. Molecular hydrogen has been shown to attenuate oxidative stress and improve lipid, glucose and energy metabolism in patients and animal models of hepatic steatosis and atherosclerosis, but the underlying molecular mechanisms remain largely unknown.

Methods

Human hepatoma HepG2 cells were exposed to palmitate-BSA complex after treatment with or without hydrogen for 24 h. The fatty acid uptake was measured by using spectrofluorometry and the lipid content was detected by Oil Red O staining. JNK phosphorylation and CD36 expression were analyzed by Western blot and real-time PCR analyses.

Results

Pretreatment with hydrogen reduced fatty acid uptake and lipid accumulation after palmitate overload in HepG2 cells, which was associated with inhibition of JNK activation. Hydrogen treatment did not alter CD36 mRNA expression but reduced CD36 protein expression.

Conclusion

Hydrogen inhibits fatty acid uptake and lipid accumulation through the downregulation of CD36 at the protein level in hepatic cultured cells, providing insights into the molecular mechanism underlying the hydrogen effects in vivo on lipid metabolism disorders.

Keywords:
Molecular hydrogen; HepG2 cells; Fatty acid; JNK; Phosphorylation; CD36; Hepatic steatosis