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用胰岛激活蛋白(IAP)处理的KK小鼠外周葡萄糖利用率提高,肝糖原合成受到抑制。

Enhanced peripheral glucose utilization and suppressed hepatic glycogen synthesis in KK mice treated with islet-activating protein (IAP).

作者信息

Okamoto T, Yajima M

出版信息

J Pharmacobiodyn. 1982 Mar;5(3):148-54. doi: 10.1248/bpb1978.5.148.

Abstract

Effect of islet-activating protein (IAP) on glucose utilization of peripheral tissues and glycogen synthesis of the liver was investigated in diabetic KK mice. The 14C-content of diaphragm glycogen following the injection of [U-14C] glucose was much less in KK mice than in dd/Y mice, and it was restored to normal in KK mice treated with IAP. The enhanced glucose utilization in these mice was completely abolished by the injection of anti-insulin serum. Glycogen synthesis of the liver after glucose load was also less in KK mice than in dd/Y mice, and it was clearly suppressed in both groups of mice by IAP treatment. It was concluded that improved glucose tolerance of IAP-treated KK mice was mostly due to enhanced glucose utilization of peripheral tissues secondary to increased insulin secretion induced by IAP injection.

摘要

在糖尿病KK小鼠中研究了胰岛激活蛋白(IAP)对周围组织葡萄糖利用及肝脏糖原合成的影响。注射[U-14C]葡萄糖后,KK小鼠膈肌糖原的14C含量远低于dd/Y小鼠,而经IAP治疗的KK小鼠该含量恢复至正常。注射抗胰岛素血清可完全消除这些小鼠增强的葡萄糖利用。葡萄糖负荷后KK小鼠肝脏的糖原合成也低于dd/Y小鼠,IAP治疗明显抑制了两组小鼠的糖原合成。得出的结论是,IAP治疗的KK小鼠葡萄糖耐量改善主要是由于IAP注射诱导胰岛素分泌增加继发周围组织葡萄糖利用增强。

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