Intragastric Administration of Allyl Isothiocyanate Reduces Hyperglycemia in Intraperitoneal Glucose Tolerance Test (IPGTT) by Enhancing Blood Glucose Consumption in Mice
Intragastric Administration of Allyl Isothiocyanate Reduces Hyperglycemia in Intraperitoneal Glucose Tolerance Test (IPGTT) by Enhancing Blood Glucose Consumption in Mice
复制标题
DOI：
10.3177/jnsv.59.56
复制
发表时间：
2013-02-01
影响因子：
1.6
通讯作者：
Fushiki, Tohru
中科院分区：
文献类型：
--
作者：
Mori, Noriyuki;Kurata, Manami;Fushiki, Tohru
我们通过腹腔葡萄糖耐量试验研究了异硫氰酸烯丙酯（AITC）对小鼠血糖水平的影响。与对照组相比，腹腔给药2 g/kg体重葡萄糖后，灌胃25 mg/kg体重AITC可降低血糖水平的升高。为了阐明还原的机制，使用c -13标记的葡萄糖进行了呼吸气体分析。腹腔注射c -13标记葡萄糖后，与对照相比，腹腔注射AITC增加了(CO2)-C-13的排放量。这表明AITC增加了外源性给药葡萄糖的利用，即血液中过量的葡萄糖。为了研究瞬时受体电位（TRP）通道是否介导了血糖水平的降低，我们使用了TRPA1和TRPV1敲除（KO）小鼠。灌胃AITC可以降低TRPA1 KO小鼠的血糖水平升高，但对TRPV1 KO小鼠没有作用。这些发现表明，饮食中的AITC可能通过激活TRPV1来增加对血液中过量葡萄糖的利用，从而降低血糖水平的升高。
We investigated the effects of allyl isothiocyanate (AITC) on the blood glucose levels of mice using an intraperitoneal glucose tolerance test. The intragastric administration of 25 mg/kg body weight AITC reduced the increase in blood glucose level after 2 g/kg body weight glucose was given intraperitoneally, compared with that of control mice. To elucidate the mechanism responsible for the reduction, respiratory gas analysis employing C-13-labeled glucose was performed. The intragastrically administering AITC increased (CO2)-C-13 emission, compared to vehicle, after intraperitoneal administration of C-13-labeled glucose. This indicated that AITC increased the utilization of exogenously administered glucose, which was excessive glucose in the blood. To examine whether transient receptor potential (TRP) channels mediated this reduction in the blood glucose levels, we used TRPA1 and TRPV1 knockout (KO) mice. Intragastrically administering AITC reduced the increase in the blood glucose level in TRPA1 KO mice but not in TRPV1 KO mice. These findings suggest that dietary AITC might reduce the increases in blood glucose levels by increasing the utilization of excessive glucose in the blood by activating TRPV1.