Centre for Biological Sciences, Department of Biochemistry, K.S. Rangasamy College of Arts and Science (Autonomous), Tiruchengode-637215, Namakkal District Tamilanadu, India.
Cardiovasc Hematol Agents Med Chem. 2020;18(1):37-44. doi: 10.2174/1871525718666200131121419.
The present study was conducted to evaluate the mitigating effects of Asiatic Acid (AA), on the changes in carbohydrate metabolism, insulin signaling molecules and renal function markers in Streptozotocin (STZ)-Nicotinamide (NAD) induced diabetic rats.
AA (20 mg/kg BW) was supplemented orally to the diabetic rats for 42 days. The levels of plasma glucose, Hemoglobin (Hb), glycosylated hemoglobin (HbA1c) insulin and renal function markers, carbohydrate metabolic enzymes in the kidney and insulin signaling molecules in skeletal muscle were measured.
The administration of AA elicited a significant decrease in the levels of plasma glucose, insulin resistance, HbA1c, urea, uric acid, creatinine, glycogen, glycogen synthase, glucose-6- phosphatase, and fructose-1,6-bisphosphatase and a significant increase of body weight development, insulin, Hb, hexokinase, and glycogen phosphorylase and mRNA expressions of insulin signaling molecule like insulin receptor 1, insulin receptor 2 and glucose transporter-4 in the STZ-NAD induced diabetic rats. Further, the protective effect of AA was evidenced by its histological annotation of the kidney tissues.
Hence, this study concluded that AA can protect against renal dysfunction by attenuating carbohydrate metabolic disorder and subsequently enhances glucose utilization and renal function in STZ-NAD-induced diabetic rats.
本研究旨在评估齐墩果酸(AA)对链脲佐菌素(STZ)-烟酰胺(NAD)诱导的糖尿病大鼠糖代谢、胰岛素信号分子和肾功能标志物变化的缓解作用。
AA(20mg/kgBW)经口补充至糖尿病大鼠,持续 42 天。测量血浆葡萄糖、血红蛋白(Hb)、糖化血红蛋白(HbA1c)、胰岛素和肾功能标志物、肾脏中糖代谢酶以及骨骼肌中胰岛素信号分子的水平。
AA 的给药显著降低了血浆葡萄糖、胰岛素抵抗、HbA1c、尿素、尿酸、肌酐、糖原、糖原合酶、葡萄糖-6-磷酸酶和果糖-1,6-二磷酸酶的水平,显著增加了体重发育、胰岛素、Hb、己糖激酶和糖原磷酸化酶的水平,并显著增加了胰岛素信号分子如胰岛素受体 1、胰岛素受体 2 和葡萄糖转运蛋白-4 的 mRNA 表达在 STZ-NAD 诱导的糖尿病大鼠中。此外,AA 的保护作用通过其对肾脏组织的组织学注释得到了证实。
因此,本研究得出结论,AA 可以通过减轻糖代谢紊乱来保护肾脏功能,从而增强 STZ-NAD 诱导的糖尿病大鼠的葡萄糖利用和肾功能。