Isosativan from the Nigerian Propolis Activates the mTORC2/AKT Pathway and Suppresses Muscle Atrophy Genes Atrogin-1 and MuRF1 in Diabetic Rats
Abstract
Objective: The study investigated the effects of Isosativan on the mTORC2/AKT pathway and diabetic muscle atrophy in a rat model of the disease.
Material and Methods: Diabetes was induced by a high-fat diet and administration of a low-dose streptozotocin injection. The animals confirmed to be diabetic were subsequently treated with Isosativan (50 mg/kg) and their responses were evaluated based on muscle atrophy and body weight. Key biochemical pathways were assessed, particularly the mTORC2/AKT signaling pathway and the muscle atrophy genes Atrogin-1 and MuRF1, in order to determine the mechanism underlying the effects of this Isosativan.
Results: Administration of Isosativan resulted in significant improvements in diabetic muscle atrophy. The treated rats exhibited increased levels of the mTORC2 and AKT proteins and maintained relatively higher body weights compared to untreated diabetic controls. The muscle atrophy-related genes, Atrogin-1 and MuRF1, were also significantly suppressed in the treated group.
Conclusion: Isosativan shows promise as a therapeutic agent for combating diabetes and diabetic muscle atrophy, operating through the activation of the mTORC2/AKT pathway, thereby leading to better utilization of glucose. This finding suggests that Isosativan could be a viable treatment option for managing diabetes-related metabolic problems, offering a novel approach for therapeutic intervention in diabetic muscle atrophy.
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