Key result
Ginsenoside Rg5 alleviated hepatic insulin resistance and improved glucose intolerance in diabetic db/db mice by activating the IRS1/PI3K/AKT/GSK3β-GS signaling pathway.
Why the study?
Does Ginsenoside Rg5 improve hepatic insulin resistance and glucose intolerance in diabetic db/db mice?
Does Ginsenoside Rg5 improve hepatic insulin resistance and glucose intolerance in diabetic db/db mice?
Ginsenoside Rg5 demonstrates potential as a treatment for type 2 diabetes by alleviating hepatic insulin resistance and improving glucose intolerance via the IRS1/PI3K/AKT/GSK3β-GS signaling pathway in a mouse model.
Should not change diabetes practice; leaves open translation of this pathway effect to humans.
Type 2 diabetes mellitus (T2DM) is a systemic metabolic disorder that has become a major threat to public health. Ginsenoside Rg5 (Rg5) has a putative hypoglycemic effect, but its potential mechanism remains unclear. Here, we found that Rg5 not only reduced glycolipid parameters (FBG, TC, TG, and LDL-C), relieved inflammation (TNF-α, IL-6, and IL-1β), improved hepatic lipid accumulation, and repaired pancreas damage but also increased hepatic glycogen storage by reducing the expression of GSK-3β and increasing the expression of GS in diabetic db/db mice. Furthermore, Rg5 significantly up-regulated the phosphorylation of IRS1, PI3K, and AKT to enhance insulin transduction in liver tissues. These results indicated that Rg5 could alleviate hepatic insulin resistance and improve glucose intolerance by activating the IRS1/PI3K/AKT/GSK3β-GS signaling pathway. Together, Rg5 provide a potential treatment for T2DM and its related metabolic disorders.
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Wei et al. (2020) studied Type 2 diabetes mellitus. Ginsenoside Rg5 was evaluated on Hepatic insulin resistance and glucose intolerance. Ginsenoside Rg5 alleviated hepatic insulin resistance and improved glucose intolerance in diabetic db/db mice by activating the IRS1/PI3K/AKT/GSK3β-GS signaling pathway.
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