• 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

四氧嘧啶和胰岛素对大鼠脑内碳水化合物代谢的影响。

Effect of alloxan and insulin on carbohydrate metabolism in rat brain.

作者信息

Rinaudo M T, Ponzetto C, Curto M, Bruno R

出版信息

Ital J Biochem. 1978 May-Jun;27(3):177-90.

PMID:738860
Abstract

8 and 24 hours after alloxan administration, diabetic rat brain shows decreased glycogen content, significantly increased FDP, triose phosphates, pyruvate and lactate levels, a large rise in glucose and a 27% activation of anaerobic lactate production from glycogen. 48 hours after alloxan administration there is a recovery of glycogen and a fall in lactate levels. ATP and AMP levels are unchanged 8 and 24 hours after alloxan administration but the former is increased and the latter decreased 48 hours posttreatment. Insulin given to rats 8 hours after alloxan treatment reverses glycogen, FDP, triose phosphates, pyruvate and lactate levels seen in the diabetic rat brain. In addition the increament in glucose is reduced by half and the rate of anaerobic lactate formation from glycogen is restored to control values. G-6-P levels, unaffected by alloxan or insulin alone, are significantly lowered in animals which received insulin after alloxan. Phosphorylase, HK, PFK, ALD, GAPDH, PK, LDH and Glycogen synthetase activities are not modified in rat brain by administration of alloxan or insulin or both.

摘要

给予四氧嘧啶后8小时和24小时,糖尿病大鼠脑内糖原含量降低,1,6 - 二磷酸果糖(FDP)、磷酸丙糖、丙酮酸和乳酸水平显著升高,葡萄糖大幅增加,糖原无氧酵解生成乳酸的过程激活了27%。给予四氧嘧啶后48小时,糖原恢复,乳酸水平下降。给予四氧嘧啶后8小时和24小时,三磷酸腺苷(ATP)和一磷酸腺苷(AMP)水平未发生变化,但治疗后48小时,前者升高,后者降低。在给予四氧嘧啶8小时后给大鼠注射胰岛素,可逆转糖尿病大鼠脑内糖原、FDP、磷酸丙糖、丙酮酸和乳酸水平。此外,葡萄糖的增加量减半,糖原无氧酵解生成乳酸的速率恢复至对照值。单独使用四氧嘧啶或胰岛素对6 - 磷酸葡萄糖(G - 6 - P)水平无影响,但在给予四氧嘧啶后再注射胰岛素的动物中,G - 6 - P水平显著降低。给予四氧嘧啶、胰岛素或两者同时给药,均不会改变大鼠脑内磷酸化酶、己糖激酶(HK)、磷酸果糖激酶(PFK)、醛缩酶(ALD)、甘油醛 - 3 - 磷酸脱氢酶(GAPDH)、丙酮酸激酶(PK)、乳酸脱氢酶(LDH)和糖原合成酶的活性。

相似文献

1
Effect of alloxan and insulin on carbohydrate metabolism in rat brain.四氧嘧啶和胰岛素对大鼠脑内碳水化合物代谢的影响。
Ital J Biochem. 1978 May-Jun;27(3):177-90.
2
Proceedings: Rat brain sugar metabolism following alloxan-induced diabetes.论文集:四氧嘧啶诱导糖尿病后大鼠脑糖代谢
Ital J Biochem. 1976 Mar-Apr;25(2):178-9.
3
Relative contribution of glycogen synthesis and glycolysis to insulin-mediated glucose uptake. A dose-response euglycemic clamp study in normal and diabetic rats.糖原合成与糖酵解对胰岛素介导的葡萄糖摄取的相对贡献。正常和糖尿病大鼠的剂量反应性正常血糖钳夹研究。
J Clin Invest. 1990 Jun;85(6):1785-92. doi: 10.1172/JCI114636.
4
Measurement of concentrations of metabolites in adipose tissue and effects of insulin, alloxan-diabetes and adrenaline.脂肪组织中代谢物浓度的测量以及胰岛素、四氧嘧啶糖尿病和肾上腺素的影响。
Biochem J. 1966 Aug;100(2):407-19. doi: 10.1042/bj1000407.
5
Effects of increased heart work on glycolysis and adenine nucleotides in the perfused heart of normal and diabetic rats.增加心脏工作对正常和糖尿病大鼠灌注心脏中糖酵解和腺嘌呤核苷酸的影响。
Biochem J. 1971 Sep;124(3):475-90. doi: 10.1042/bj1240475.
6
[Insulin sensitivity of isolated muscle tissue of rats with manifest alloxan diabetes of different duration].[不同病程明显的四氧嘧啶糖尿病大鼠离体肌肉组织的胰岛素敏感性]
Biull Eksp Biol Med. 1979 Oct;88(10):412-4.
7
[Brain sugar metabolism in alloxan diabetic rats (author's transl)].四氧嘧啶糖尿病大鼠的脑糖代谢(作者译)
Pathologica. 1980 Jul-Aug;72(1020):555-66.
8
Carbohydrate metabolism in normal and diabetic rats following long-term oral trypsin inhibitor administration.长期口服胰蛋白酶抑制剂后正常及糖尿病大鼠的碳水化合物代谢
Scand J Gastroenterol. 1976;11(4):369-75.
9
Placental glycogen metabolism in diabetic pregnancy.糖尿病妊娠中的胎盘糖原代谢
Isr J Med Sci. 1991 Aug-Sep;27(8-9):449-61.
10
Effects of alloxan diabetes, anti-insulin serum diabetes, and non-diabetic dehydration on brain carbohydrate and energy metabolism in young mice.四氧嘧啶糖尿病、抗胰岛素血清糖尿病及非糖尿病性脱水对幼鼠脑碳水化合物和能量代谢的影响。
J Biol Chem. 1975 Mar 10;250(5):1751-8.