Masukawa T, Nakanishi K
Department of Clinical Biochemistry, Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Jpn J Pharmacol. 1994 Sep;66(1):159-61. doi: 10.1254/jjp.66.159.
Dimethylthiourea (DMTU, 4.0 mmol/kg) injected into mice 30 min prior to alloxan injection markedly protected mice against the diabetogenic actions of 75 mg/kg alloxan. At 30 min after the above dose of DMTU alone (no alloxan), there was a marked rise in blood glucose. Mannoheptulose, an antagonist of glucose action at pancreatic beta-cells, when given 24 min after DMTU and 6 min before alloxan, eliminated the DMTU-induced protection. The protection was also removed in the fasted mice in which DMTU did not cause hyperglycemia. These results indicate that DMTU protected mice from alloxan-induced diabetes by the indirect mechanism of producing hyperglycemia at the time of alloxan injection.
在注射四氧嘧啶前30分钟给小鼠注射二甲基硫脲(DMTU,4.0 mmol/kg),可显著保护小鼠免受75 mg/kg四氧嘧啶的致糖尿病作用。单独给予上述剂量的DMTU(无四氧嘧啶)30分钟后,血糖显著升高。甘露庚酮糖是葡萄糖对胰腺β细胞作用的拮抗剂,在DMTU给药24分钟后且在四氧嘧啶给药前6分钟给予时,可消除DMTU诱导的保护作用。在禁食小鼠中,DMTU不会引起高血糖,其保护作用也会消失。这些结果表明,DMTU通过在注射四氧嘧啶时产生高血糖的间接机制保护小鼠免受四氧嘧啶诱导的糖尿病。