Molecular hydrogen improves type 2 diabetes through inhibiting oxidative stress.

Abstract

Using a rat model of type 2 diabetes mellitus (T2DM) established by high-fat diet feeding followed by streptozotocin injection (30 mg/kg via caudal vein) in Sprague-Dawley rats, this study examined the effects of molecular hydrogen over an 80-day period. Biochemical measurements included fasting blood glucose, blood lipids, hepatic glycogen, insulin sensitivity index, insulin resistance index, serum superoxide dismutase (SOD), and malondialdehyde (MDA). Molecular hydrogen administration was associated with reductions in fasting blood glucose, enhanced hepatic glycogen synthesis, and improved insulin sensitivity. SOD levels increased while MDA levels declined, indicating reduced oxidative stress. Histological examination revealed attenuation of pathological changes in pancreatic islets and kidney tissue. Western blot analysis showed decreased expression of TLR4 and MyD88, along with reduced phosphorylation of p65 and IκB, implicating the TLR4/MyD88/NF-κB signaling axis as a key mechanistic pathway. Note: this article has been retracted.

Mechanism

Molecular hydrogen suppresses the TLR4/MyD88/NF-κB signaling pathway by downregulating TLR4 and MyD88 expression and reducing phosphorylation of p65 and IκB, thereby attenuating oxidative stress in diabetic rats.