Hydrogen Water Protects Kidneys from Diabetes-Related Damage in Study
- Authors
- Masanori Katakura, Michio Hashimoto, Yoko Tanabe, Osamu Shido
- Journal
- Medical Gas Research
- Year
- 2012
- DOI
- 10.1186/2045-9912-2-18
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Type 2 Diabetes
- Body System
- Renal
TL;DR
Drinking hydrogen-rich water may help reduce kidney damage caused by high blood sugar and harmful compounds in rats with conditions similar to human diabetes and metabolic syndrome.
Key Finding
Hydrogen-rich water reduced reactive oxygen species production by 34% in the kidneys of rats with metabolic syndrome and decreased harmful glucose-related compounds by 60-81%.
Summary
This study tested whether hydrogen-rich water could reduce harmful molecules called reactive oxygen species (ROS) in kidney tissue. Researchers used rats with metabolic syndrome (a condition involving obesity and blood sugar problems) and gave some of them hydrogen-rich water for 16 weeks. They found that hydrogen-rich water decreased ROS production by 34% and significantly reduced other harmful compounds in the kidneys.
Practical Takeaway
While this animal study suggests hydrogen-rich water may help protect kidneys from oxidative damage related to metabolic syndrome, these results cannot yet be applied to humans. Further research in human subjects would be needed to determine whether hydrogen-rich water offers similar benefits for people with type 2 diabetes or metabolic syndrome.
Abstract
Reactive oxygen species (ROS) production induced by α,β-dicarbonyl compounds and advanced glycation end products causes renal dysfunction in patients with type 2 diabetes and metabolic syndrome. Hydrogen-rich water (HRW) increases the H2 level in blood and tissues, thus reducing oxidative stress in animals as well as humans. In this study, we investigated the effects of HRW on glucose- and α,β-dicarbonyl compound-induced ROS generation in vitro and in vivo. Kidney homogenates from Wistar rats were incubated in vitro with glucose and α,β-dicarbonyl compounds containing HRW, following which ROS levels were measured. In vivo animal models of metabolic syndrome, SHR.Cg-Leprcp/NDmcr rats, were treated with HRW for 16 weeks, following which renal ROS production and plasma and renal α,β-dicarbonyl compound levels were measured by liquid chromatograph mass spectrometer. HRW inhibited glucose- and α,β-dicarbonyl compound-induced ROS production in kidney homogenates from Wistar rats in vitro. Furthermore, SHR.Cg-Leprcp/NDmcr rats treated with HRW showed a 34% decrease in ROS production. Moreover, their renal glyoxal, methylglyoxal, and 3-deoxyglucosone levels decreased by 81%, 77%, and 60%, respectively. Positive correlations were found between renal ROS levels and renal glyoxal (r = 0.659, p = 0.008) and methylglyoxal (r = 0.782, p = 0.001) levels. These results indicate that HRW inhibits the production of α,β-dicarbonyl compounds and ROS in the kidneys of SHR.Cg-Leprcp/NDmcr rats. Therefore, it has therapeutic potential for renal dysfunction in patient with type 2 diabetes and metabolic syndrome.