Hydrogen Therapy Improves Blood Sugar Control in Type 1 Diabetes Study
- Authors
- Haruka Amitani, Akihiro Asakawa, Kaichun Cheng, Marie Amitani, Kaori Kaimoto, Masako Nakano, Miharu Ushikai, Yingxiao Li, Minglun Tsai, Jiang-Bo Li, Mutsumi Terashi, Huhe Chaolu, Ryozo Kamimura, Akio Inui
- Journal
- PLoS One
- Year
- 2013
- DOI
- 10.1371/journal.pone.0053913
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Type 1 Diabetes
- Body System
- Endocrine
TL;DR
Hydrogen gas can help sugar enter muscle cells like insulin does and might be a new oral treatment for type 1 diabetes, but it doesn't work as well for type 2 diabetes.
Key Finding
Hydrogen gas improved blood sugar control in type 1 diabetic mice by promoting glucose uptake into skeletal muscle through insulin-like mechanisms, but showed limited effectiveness in type 2 diabetes and obesity models.
Summary
Researchers tested whether hydrogen gas could help control blood sugar in diabetic mice by studying how it affects glucose (sugar) movement into muscle cells. They found that hydrogen promoted glucose uptake into muscle cells through activation of specific cellular pathways, similar to how insulin works. In mice with type 1 diabetes, hydrogen administration improved blood sugar control, but it was less effective in mice with type 2 diabetes or obesity.
Practical Takeaway
This is an animal study only, so results cannot yet be applied to humans. The findings suggest hydrogen water may have potential as a type 1 diabetes therapy, but much more research—including human clinical trials—would be needed before any health claims could be made. The lack of effectiveness in type 2 diabetes models is also an important limitation to note.
Abstract
Hydrogen (H(2)) acts as a therapeutic antioxidant. However, there are few reports on H(2) function in other capacities in diabetes mellitus (DM). Therefore, in this study, we investigated the role of H(2) in glucose transport by studying cultured mouse C2C12 cells and human hepatoma Hep-G2 cells in vitro, in addition to three types of diabetic mice [Streptozotocin (STZ)-induced type 1 diabetic mice, high-fat diet-induced type 2 diabetic mice, and genetically diabetic db/db mice] in vivo. The results show that H(2) promoted 2-[(14)C]-deoxy-d-glucose (2-DG) uptake into C2C12 cells via the translocation of glucose transporter Glut4 through activation of phosphatidylinositol-3-OH kinase (PI3K), protein kinase C (PKC), and AMP-activated protein kinase (AMPK), although it did not stimulate the translocation of Glut2 in Hep G2 cells. H(2) significantly increased skeletal muscle membrane Glut4 expression and markedly improved glycemic control in STZ-induced type 1 diabetic mice after chronic intraperitoneal (i.p.) and oral (p.o.) administration. However, long-term p.o. administration of H(2) had least effect on the obese and non-insulin-dependent type 2 diabetes mouse models. Our study demonstrates that H(2) exerts metabolic effects similar to those of insulin and may be a novel therapeutic alternative to insulin in type 1 diabetes mellitus that can be administered orally.