• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

神经系统和激素对喂食大鼠2-脱氧-D-葡萄糖诱导的高血糖的相对重要性。

The relative importance of nervous system and hormones to the 2-deoxy-D-glucose-induced hyperglycemia in fed rats.

作者信息

Matsunaga H, Iguchi A, Yatomi A, Uemura K, Miura H, Gotoh M, Mano T, Sakamoto N

机构信息

Third Department of Internal Medicine, Nagoya University School of Medicine, Japan.

出版信息

Endocrinology. 1989 Mar;124(3):1259-64. doi: 10.1210/endo-124-3-1259.

DOI:10.1210/endo-124-3-1259
PMID:2563682
Abstract

We examined the relative contributions of hormones and nervous system to the total 2-deoxy-D-glucose (2-DG)-induced central nervous system-mediated hyperglycemia. 2-DG was injected into the third cerebral ventricle in the following four groups of rats, and hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were measured: 1) intact rats; 2) intact rats receiving somatostatin with insulin infusion through the femoral vein to inhibit glucagon secretion and maintain the basal insulin level; 3) bilateral adrenalectomized (ADX) rats to prevent epinephrine secretion; and 4) ADX rats receiving somatostatin with insulin infusion. Comparing areas under glucose curves among the intact rats, those receiving somatostatin with insulin infusion, ADX rats, and ADX rats receiving somatostatin with insulin infusion, the area under the glucose curve was intact rats greater than intact rats receiving somatostatin with insulin infusion greater than ADX rats receiving somatostatin with insulin infusion greater than ADX rats. These results suggest that there are three distinct sympathetic nervous system responses to 2-DG-induced central nervous system-mediated hyperglycemia. 2-DG-induced hyperglycemia is not dependent on only one of those three systems, it is dependent on all of them. The relative potency of the factors to 2-DG-induced hyperglycemia increases in the following order: direct neural innervation of liver (including suppressive epinephrine action on insulin secretion), glucagon, and direct epinephrine action on liver.

摘要

我们研究了激素和神经系统对2-脱氧-D-葡萄糖(2-DG)诱导的中枢神经系统介导的高血糖症的相对贡献。将2-DG注入以下四组大鼠的第三脑室,并测量肝静脉血浆葡萄糖、免疫反应性胰高血糖素、免疫反应性胰岛素、肾上腺素和去甲肾上腺素:1)完整大鼠;2)通过股静脉输注胰岛素并接受生长抑素的完整大鼠,以抑制胰高血糖素分泌并维持基础胰岛素水平;3)双侧肾上腺切除(ADX)大鼠以防止肾上腺素分泌;4)接受生长抑素并输注胰岛素的ADX大鼠。比较完整大鼠、接受生长抑素并输注胰岛素的大鼠、ADX大鼠以及接受生长抑素并输注胰岛素的ADX大鼠的葡萄糖曲线下面积,葡萄糖曲线下面积的顺序为:完整大鼠大于接受生长抑素并输注胰岛素的完整大鼠大于接受生长抑素并输注胰岛素的ADX大鼠大于ADX大鼠。这些结果表明,对于2-DG诱导的中枢神经系统介导的高血糖症存在三种不同的交感神经系统反应。2-DG诱导的高血糖症并非仅依赖于这三个系统中的一个,而是依赖于所有这些系统。这些因素对2-DG诱导的高血糖症的相对效力按以下顺序增加:肝脏的直接神经支配(包括肾上腺素对胰岛素分泌的抑制作用)、胰高血糖素以及肾上腺素对肝脏的直接作用。

相似文献

1
The relative importance of nervous system and hormones to the 2-deoxy-D-glucose-induced hyperglycemia in fed rats.神经系统和激素对喂食大鼠2-脱氧-D-葡萄糖诱导的高血糖的相对重要性。
Endocrinology. 1989 Mar;124(3):1259-64. doi: 10.1210/endo-124-3-1259.
2
Relative contribution of nervous system and hormones to hyperglycemia induced by thyrotropin-releasing hormone in fed rats.促甲状腺激素释放激素诱导的进食大鼠高血糖症中神经系统和激素的相对作用
Neuroendocrinology. 1991 Jul;54(1):1-6. doi: 10.1159/000125843.
3
Relative contributions of the nervous system and hormones to CNS-mediated hyperglycemia.神经系统和激素对中枢神经系统介导的高血糖的相对作用。
Am J Physiol. 1988 Dec;255(6 Pt 1):E920-7. doi: 10.1152/ajpendo.1988.255.6.E920.
4
Mechanism of intrahippocampal neostigmine-induced hyperglycemia in fed rats.喂食大鼠海马内新斯的明诱导高血糖的机制。
Neuroendocrinology. 1992 Jan;55(1):44-50. doi: 10.1159/000126095.
5
Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats.新斯的明诱导的高血糖症由进食大鼠的中枢毒蕈碱受体介导。
Brain Res. 1990 Jan 22;507(2):295-300. doi: 10.1016/0006-8993(90)90285-j.
6
Relative contribution of nervous system and hormones to CNS-mediated hyperglycemia is determined by the neurochemical specificity in the brain.神经系统和激素对中枢神经系统介导的高血糖的相对贡献由大脑中的神经化学特异性决定。
Physiol Behav. 1991 Nov;50(5):1019-25. doi: 10.1016/0031-9384(91)90431-m.
7
Bicuculline methiodide influences the central nervous system to produce hyperglycemia in rats.美索比妥影响大鼠中枢神经系统,使其产生高血糖症。
J Neuroendocrinol. 1994 Aug;6(4):443-6. doi: 10.1111/j.1365-2826.1994.tb00605.x.
8
2-deoxy-D-glucose-induced hyperglycemia: role for direct sympathetic nervous system activation of liver glucose output.
Brain Res. 1989 Dec 25;505(1):23-8. doi: 10.1016/0006-8993(89)90111-x.
9
Prostaglandins affect the central nervous system to produce hyperglycemia in rats.前列腺素影响中枢神经系统,使大鼠产生高血糖。
Endocrinology. 1987 Jul;121(1):36-41. doi: 10.1210/endo-121-1-36.
10
Neither adrenergic nor cholinergic antagonists in the central nervous system affect 2-deoxy-D-glucose(2-DG)-induced hyperglycemia.
Brain Res. 1990 Mar 5;510(2):321-5. doi: 10.1016/0006-8993(90)91383-r.

引用本文的文献

1
An exploration of the aversive properties of 2-deoxy-D-glucose in rats.探讨 2-脱氧-D-葡萄糖在大鼠体内的厌恶特性。
Psychopharmacology (Berl). 2018 Oct;235(10):3055-3063. doi: 10.1007/s00213-018-4998-1. Epub 2018 Aug 15.
2
Derivation and Validation of a Mortality Risk Score for Severe Hand, Foot and Mouth Disease in China.中国重症手足口病死亡率评分的推导和验证。
Sci Rep. 2017 Jun 13;7(1):3371. doi: 10.1038/s41598-017-02658-4.
3
Effects of pharmacological doses of 2-deoxyglucose on plasma catecholamines and glucose levels in patients with schizophrenia.
药理剂量的2-脱氧葡萄糖对精神分裂症患者血浆儿茶酚胺和血糖水平的影响。
Psychopharmacology (Berl). 2004 Nov;176(3-4):369-75. doi: 10.1007/s00213-004-1890-y. Epub 2004 Jun 4.
4
Metabolic responses to glucoprivation induced by 2-deoxy-D-glucose in Brycon cephalus (Teleostei, Characidae).
J Comp Physiol B. 2004 Jan;174(1):91-6. doi: 10.1007/s00360-003-0392-2. Epub 2003 Oct 28.
5
Contribution of adrenergic nerves and the adrenals to 2-deoxy-D-glucose-induced insulin and glucagon secretion in the mouse.
Int J Pancreatol. 1991 Nov-Dec;10(3-4):207-15. doi: 10.1007/BF02924158.