Calenduloside E produced by Bifidobacterium animalis B960 enhanced glibenclamide efficacy and alleviated the drug adverse effects in a type 2 diabetes model via the IRS1/PI3K/AKT signaling pathway

Type 2 diabetes is a prevalent metabolic disorder characterized by insulin resistance and relative insulin deficiency. Glibenclamide is a commonly used sulfonylurea drug for its treatment, yet it comes with limitations such as potential hypoglycemia and weight gain, along with a gradual decline in efficacy over time.In recent research, Bifidobacterium animalis B960 has drawn attention for its unique metabolite, Calenduloside E. This compound shows promise in enhancing the efficacy of glibenclamide and alleviating its adverse effects in a type 2 diabetes model. The IRS1/PI3K/AKT signaling pathway, a key regulator in insulin signaling, is found to be involved in this process. Calenduloside E is thought to modulate this pathway, promoting insulin sensitivity and glucose uptake in target tissues. By doing so, it not only boosts the anti - diabetic effect of glibenclamide but also mitigates issues like hypoglycemia and weight - related side - effects.These findings offer new insights into improving the treatment of type 2 diabetes. The combination of Calenduloside E and glibenclamide may represent a novel approach to enhance therapeutic outcomes while reducing the drawbacks associated with traditional monotherapy. Future research is warranted to further explore the underlying mechanisms and potential applications of this combination in clinical settings.