Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, Chuncheon 200-702, Korea.
Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Hallym University, Chuncheon 200-702, Korea.
Korean J Physiol Pharmacol. 2014 Feb;18(1):41-6. doi: 10.4196/kjpp.2014.18.1.41. Epub 2014 Feb 13.
The possible roles of spinal histamine receptors in the regulation of the blood glucose level were studied in ICR mice. Mice were intrathecally (i.t.) treated with histamine 1 (H1) receptor agonist (2-pyridylethylamine) or antagonist (cetirizine), histamine 2 (H2) receptor agonist (dimaprit) or antagonist (ranitidine), histamine 3 (H3) receptor agonist (α-methylhistamine) or antagonist (carcinine) and histamine 4 (H4) receptor agonist (VUF 8430) or antagonist (JNJ 7777120), and the blood glucose level was measured at 30, 60 and 120 min after i.t. administration. The i.t. injection with α-methylhistamine, but not carcinine slightly caused an elevation of the blood glucose level. In addition, histamine H1, H2, and H4 receptor agonists and antagonists did not affect the blood glucose level. In D-glucose-fed model, i.t. pretreatment with cetirizine enhanced the blood glucose level, whereas 2-pyridylethylamine did not affect. The i.t. pretreatment with dimaprit, but not ranitidine, enhanced the blood glucose level in D-glucose-fed model. In addition, α-methylhistamine, but not carcinine, slightly but significantly enhanced the blood glucose level D-glucose-fed model. Finally, i.t. pretreatment with JNJ 7777120, but not VUF 8430, slightly but significantly increased the blood glucose level. Although histamine receptors themselves located at the spinal cord do not exert any effect on the regulation of the blood glucose level, our results suggest that the activation of spinal histamine H2 receptors and the blockade of spinal histamine H1 or H3 receptors may play modulatory roles for up-regulation and down-regulation, respectively, of the blood glucose level in D-glucose fed model.
研究了脊髓组胺受体在调节血糖水平中的可能作用。将组胺 1(H1)受体激动剂(2-吡啶乙胺)或拮抗剂(西替利嗪)、组胺 2(H2)受体激动剂(二甲普里)或拮抗剂(雷尼替丁)、组胺 3(H3)受体激动剂(α-甲基组胺)或拮抗剂(卡尼汀)和组胺 4(H4)受体激动剂(VUF 8430)或拮抗剂(JNJ 7777120)鞘内(i.t.)给予 ICR 小鼠,在 i.t. 给药后 30、60 和 120 分钟测量血糖水平。α-甲基组胺而非卡尼汀鞘内注射轻微引起血糖水平升高。此外,组胺 H1、H2 和 H4 受体激动剂和拮抗剂均不影响血糖水平。在 D-葡萄糖喂养模型中,西替利嗪的 i.t. 预处理增强了血糖水平,而 2-吡啶乙胺则没有影响。二甲普里的 i.t. 预处理增强了 D-葡萄糖喂养模型中的血糖水平,但雷尼替丁则没有。此外,α-甲基组胺而非卡尼汀轻微但显著增强了 D-葡萄糖喂养模型中的血糖水平。最后,JNJ 7777120 的 i.t. 预处理轻微但显著增加了血糖水平,但 VUF 8430 则没有。虽然位于脊髓的组胺受体本身对血糖水平的调节没有任何影响,但我们的结果表明,脊髓组胺 H2 受体的激活和组胺 H1 或 H3 受体的阻断可能分别对 D-葡萄糖喂养模型中的血糖水平上调和下调发挥调节作用。