本研究旨在研究尿囊素对大鼠高脂饮食(HFD)和链脲佐菌素(STZ)产生的糖尿病的潜在治疗作用。
■雄性Sprague-Dawley大鼠饲喂高脂肪饮食以诱导胰岛素抵抗,然后注射链脲佐菌素诱发糖尿病。通过计算代谢参数的变化来评估尿囊素(200、400和800mg/kg/天)口服治疗8周的效果,生化指标,我们进行了口服葡萄糖耐量试验(OGTT)和高胰岛素-正常血糖钳夹试验.在肝脏中进行组织病理学研究,肾脏和胰腺.接下来,通过Westernblot分析检测MAPK和胰岛素信号通路的表达,以阐明这些抗糖尿病活性的潜在机制.
■尿囊素的给药导致空腹血糖(FBG)水平显着降低,糖原水平,糖尿病大鼠的糖化血红蛋白水平。此外,尿囊素治疗导致体重增长和血清胰岛素水平的剂量依赖性增加。此外,尿囊素的给药导致糖尿病大鼠的血脂水平大大降低并改善了组织学改变。对糖尿病大鼠施用尿囊素导致丙二醛(MDA)水平显着降低,伴随着血清中抗氧化酶活性的增加,肝脏,还有肾.口服葡萄糖耐量和高胰岛素-正常血糖钳夹试验的结果表明,尿囊素给药后胰岛素抵抗显着增加。尿囊素对IRS-2/PI3K/p-Akt/GLUT表达的上调表明PI3K/Akt信号通路与尿囊素的抗高血糖活性之间存在机制关系。此外,它导致上述受糖尿病影响的大鼠组织中TGF-β1/p38MAPK/Caspase-3表达水平降低。
■本研究提示尿囊素通过激活PI3K治疗2型糖尿病。此外,它减少肝脏,肾,胰腺细胞凋亡和炎症诱导的胰岛素抵抗。re.
UNASSIGNED: The current study aimed to investigate the potential therapeutic impact of allantoin on diabetes produced by a high-fat diet (HFD) and streptozotocin (STZ) in rats.
UNASSIGNED: Male Sprague-Dawley rats were fed a high-fat diet to induce insulin resistance, followed by streptozotocin injection to induce diabetes. The effect of oral treatment of allantoin (200, 400 and 800 mg/kg/day) for 8 weeks was evaluated by calculating the alteration in metabolic parameters, biochemical indicators, the oral glucose tolerance tests (OGTT) and hyperinsulinemic-euglycemic clamp tests were performed. Histopathological studies were performed in the liver, kidney and pancreas. Next, the expressions of the MAPK and insulin signaling pathway were measured by Western blot analysis to elucidate the potential mechanism underlying these antidiabetic activities.
UNASSIGNED: The administration of allantoin resulted in a significant decrease in fasting blood glucose (FBG) levels, glycogen levels, and glycosylated hemoglobin levels in diabetic rats. Additionally, allantoin therapy led to a dose-dependent increase in body weight growth and serum insulin levels. In addition, the administration of allantoin resulted in a considerable reduction in lipid profile levels and amelioration of histological alterations in rats with diabetes. The administration of allantoin to diabetic rats resulted in a notable decrease in Malondialdehyde (MDA) levels, accompanied by an increase in the activity of antioxidant enzymes in the serum, liver, and kidney. The findings of oral glucose tolerance and hyperinsulinemic-euglycemic clamp tests demonstrated a significant rise in insulin resistance following the administration of allantoin. The upregulation of IRS-2/PI3K/p-Akt/GLUT expression by allantoin suggests a mechanistic relationship between the PI3K/Akt signaling pathway and the antihyperglycemic activity of allantoin. Furthermore, it resulted in a reduction in the levels of TGF-β1/p38MAPK/Caspase-3 expression in the aforementioned rat tissues affected by diabetes.
UNASSIGNED: This study implies that allantoin treats type 2 diabetes by activating PI3K. Additionally, it reduces liver, kidney, and pancreatic apoptosis and inflammation-induced insulin resistance.re.