Hydrogen Therapy Reduces Fat Storage in Liver Cells
- Authors
- Akio Iio, Mikako Ito, Tomohiro Itoh, Riyako Terazawa, Yasunori Fujita, Yoshinori Nozawa, Ikuroh Ohsawa, Kinji Ohno, Masafumi Ito
- Journal
- Medical Gas Research
- Year
- 2013
- DOI
- 10.1186/2045-9912-3-6
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Fatty Liver Disease
- Body System
- Hepatic
TL;DR
Hydrogen treatment can reduce fat buildup in liver cells by decreasing the activity of a fat-transporting protein and a stress-related pathway.
Key Finding
Molecular hydrogen reduced fatty acid uptake and lipid accumulation in liver cells by decreasing CD36 protein levels on the cell surface, independent of changes in the genetic blueprint for CD36.
Summary
Researchers studied how molecular hydrogen affects liver cells' ability to take up and store fat. They exposed liver cells to excess fatty acids and found that hydrogen treatment reduced the amount of fat the cells absorbed and accumulated. This effect appeared to work by reducing the amount of a protein called CD36 (which acts as a fatty acid transporter) on the cell surface, even though the genetic instructions for making CD36 remained unchanged.
Practical Takeaway
This laboratory study in isolated liver cells suggests a potential mechanism by which hydrogen might help with fatty liver disease and obesity-related metabolic problems. However, this is very early-stage research conducted only in cultured cells, not in living organisms or humans, so it's too soon to draw conclusions about real-world benefits for people.
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.