發明
紐西蘭
594236
594236
Use of pterosin compounds for treating diabetes and obesity
臺北醫學大學
2014/08/29
蕨素化合物nstpbp168於注射、口服均能有效對抗streptozotocin 誘導之糖尿病鼠(第一型糖尿病模式)之高血糖狀態及葡萄糖不耐受性(glucose intolerance),並能提高骨骼肌細胞(differentiated C2C12 cells)葡萄糖轉運體4 (GLUT4)之運輸,增加骨骼肌細胞對葡萄糖之利用及攝入作用。在培養的肝臟細胞,168可以扭轉磷酸carboxylkinase (PEPCK) mRNA表達的增進。體外細胞培養的綜合研究結果顯示,168具有能力引發 AMPK磷酸化和改善胰島素敏感性。另一方面,研究168對於db/db糖尿病小鼠模型的長期影響,其結果呈現,經治療21天後,可有效扭轉糖尿病小鼠之糖不耐受性 (glucose intolerance) 和胰島素抵抗 (insulin resistance),證明168在2型糖尿病模式亦具有降血糖功能。168之衍生物,nstpbp169和169-glc,也已被證明可改善dexamethasone誘導的胰島素抵抗和高脂肪的飲食誘導的胰島素抵抗。本發明為應用蕨素化合物於治療1型及2型糖尿病,亦可使用於肥胖之改善。專利申請:TW 201039836,US 2010-0190732,PCT WO 2010/085811。 Both oral and injection administration of nstpbp168 effectively improved the glucose intolerance and the GLUT4 expression in STZ-induced diabetic mice. 168 is capable of reversing the increase of PEPCK mRNA expression in the cultured liver cells, indicating that the inhibition of liver gluconeogenesis may be involved in the anti-hyperglycemic effect. The glucose intolerance, insulin resistance, and hyperlipidemia was effectively improved 28 days after the treatment of 168, to show that it possesses anti-hyperglycemic effect in type 2 diabetic. Nstpbp169 and 169-glc, the derivatives of 168, have been found to possess the anti-insulin resistance effect on a dexamethasone-induced insulin resistance mouse. 169-glc could also improve the insulin resistance and hyperlipidemia in high-fat diet-induced diabetic mice. These findings indicate that 168 and its derivatives possess the potential therapeutic effects on diabetes and obesity. Patent: TW 201039836, US 2010-0190732, PCT WO 2010/085811.
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