The effect of cassia seed extract on the regulation of the LKB1–AMPK–GLUT4 signaling pathway in the skeletal muscle of diabetic rats to improve the insulin sensitivity of the skeletal muscle

过剩4 医学 卡西亚 内科学 胰岛素抵抗 内分泌学 糖尿病 链脲佐菌素 安普克 骨骼肌 胰岛素 氧化应激 生物 蛋白激酶A 生物化学 激酶 中医药 病理 替代医学
作者
Qiuying Wang,Aihua Tong,Yingying Pan,Xiandang Zhang,Wenyu Ding,Wen Xiong
出处
期刊:Diabetology & Metabolic Syndrome [Springer Nature]
卷期号:11 (1): 108-108 被引量:11
标识
DOI:10.1186/s13098-019-0504-0
摘要

Abstract Background This study aimed to observe the hypoglycemic effect of cassia seed extract in rats with type-2 diabetes mellitus and its effect on reducing insulin resistance in the skeletal muscle. Methods 50 rats were randomly divided into the normal, model, high-dose, middle-dose, and low-dose groups of cassia seed extract (n = 10 each). A high-fat diet combined with streptozotocin administration was adopted to build type 2 diabetes models. The cassia seed extract groups were fed different concentrations cassia seed extract while the normal and model groups were fed the same volume of normal saline. The weight, FINS, GIR, insulin tolerance, blood glucose and blood lipid level, oxidative stress indices and expressions related to the LKB1–AMPK–GLUT4 pathway were detected and compared between the two groups. Results Compared with the normal group, the model group showed lower weight, glucose infusion rate and expressions related to LKB1–AMPK–GLUT4 pathway and higher FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices (all P < 0.05). Compared with the model group, higher weight, glucose infusion rate and expressions related to LKB1–AMPK–GLUT4 pathway and lower FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices were observed in all groups that were administered cassia see extract (all P < 0.05). Conclusion Cassia seed extract could noticeably improve the insulin resistance of diabetic rats and enhance the insulin sensitivity of their skeletal muscles. Its mechanism may be related to damage repair of the LKB1–AMPK–GLUT4 signaling pathway and oxidative stress in the skeletal muscle.

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