Hydrogen Water Reduces Fatty Liver Disease in Mice Study
- Authors
- Xiang Wang, Jiao Wang
- Journal
- Biological Chemistry
- Year
- 2017
- DOI
- 10.1515/hsz-2017-0303
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Non-Alcoholic Fatty Liver Disease
- Body System
- Hepatic
TL;DR
Drinking water with a high concentration of hydrogen gas can help reduce liver fat and improve liver health in mice with a condition similar to human fatty liver disease.
Key Finding
In mice with diet-induced fatty liver disease, hydrogen water reduced liver damage markers and blood fat levels while activating protective cellular pathways through changes in specific gene regulators.
Summary
Researchers tested whether hydrogen-rich water could help treat fatty liver disease (a condition where fat builds up in the liver) in mice fed a high-fat diet. They found that hydrogen water reduced liver damage markers and lipid (fat) levels in the blood, and changed the activity of specific genes and proteins involved in protecting cells from damage. The effect appeared to work by reducing a molecule called miR-136, which then allowed other protective pathways to activate.
Practical Takeaway
This study is preliminary—it was conducted only in mice, not humans, and the study duration and sample size were not reported. While the results suggest hydrogen water may influence liver-protective pathways, much more research is needed before any conclusions can be drawn about its effects in people with fatty liver disease.
Abstract
Abstract This study was aimed to investigate the potential regulatory mechanism of high-content hydrogen water (HHW) in non-alcoholic fatty liver disease (NAFLD). A high-fat diet (HFD)-induced NAFLD mice model and cellular model were prepared. The serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total cholesterol (TCH) and triglycerides (TG) were measured. The expression levels of representative five microRNA (miRNAs) (miR-103, miR-488, miR-136, miR-505 and miR-148a) in liver tissues were determined by quantitative real-time PCR (qRT-PCR). The target of miR-136 was validated by RNA immunoprecipitation (RIP) and pull-down assay. MiR-136, MEG3 and nuclear factor erythroid 2-related factor 2 (Nrf2) expression levels following cell treatment were detected in hepatocytes using qRT-PCR and Western blotting. Moreover, cell viability and TG content were conducted. MiR-136 was downregulated, MEG3 as well as Nrf2 was upregulated and serum lipid level was reduced in NAFLD mice model after HHW treatment, which exerted the same effect in cellular model. RIP and RNA pull-down assay confirmed that MEG2 was a downstream target of miR-136. What’s more, HHW ameliorated lipid accumulation by regulating miR-136/MEG3/Nrf2 axis in vitro and in vivo . Hence, HHW alleviated NAFLD by downregulation of miR-136 through mediating Nrf2 via targeting MEG3.