Beneficial effect of the methanolic leaf extract of Allium hookeri on stimulating glutathione biosynthesis and preventing impaired glucose metabolism in type 2 diabetes

Oxidative stress resulting from the depletion of glutathione (GSH) level plays a vital role in generating various degenerative diseases, including type 2 diabetes (T2D). We tested the hypothesis that depleted glutathione levels can be enhanced and the impaired glucose metabolism can be prevented by supplementing Allium hookeri, a herb rich in organosulfur compounds, in a High Fat (HF) diet-induced T2D Male Sprague Dawley rat model. The experimental rats were divided into three groups (n = 6), namely normal diet, high-fat diet, and high-fat diet treated with A.hookeri methanolic leaf extract (250 mg/kg). Consumption of HF diet along with the plant extract resulted in significant reduction of the body weight (7.08%-14.89%) and blood glucose level (6.5%-16.4%) from the 13th week onward. There was a significant decrease in reactive oxygen species, oxidized glutathione (GSSG) levels, and an increase in GSH level in skeletal muscle tissues supplemented with the plant extract. The protein expressions of the signaling molecules such as GCLC and GR involved in GSH synthesis and of GLUT4 in glucose transport were also upregulated in the skeletal muscle tissues of the plant extract-treated group. Results of in vitro studies with muscle cell line (L6) further demonstrated the beneficial effect of the plant extract in increasing glucose uptake and maintaining the GSH/GSSH equilibrium via regulation of protein expression of GCLC/GR/ GLUT4 signaling molecules in sodium palmitate (0.75 mM) treated cells. Overall this study suggests that dietary supplementation with Allium hookeri, can restore the glutathione level and regulate the blood glucose level in T2D.

Automated summary

The study demonstrated that supplementation of Allium hookeri can increase glutathione levels, decrease body weight and blood glucose levels in a high-fat diet-induced type 2 diabetes rat model, and regulate glucose metabolism by modulating the expression of signaling molecules.