Substrate competition and insulin action in animal models.

R Vettor, A M Lombardi, R Fabris, R Serra, C Pagano, C Macor, G Federspil
{"title":"Substrate competition and insulin action in animal models.","authors":"R Vettor,&nbsp;A M Lombardi,&nbsp;R Fabris,&nbsp;R Serra,&nbsp;C Pagano,&nbsp;C Macor,&nbsp;G Federspil","doi":"10.1038/sj.ijo.0801271","DOIUrl":null,"url":null,"abstract":"<p><p>Increased basal plasma FFA and lactate concentrations are often present in obesity and may deeply affect insulin action. The inhibition of glucose transport or phosphorylation is thought to be involved in this phenomenon, but the molecular mechanisms on the basis are still unknown. In our laboratory we observed that a chronic infusion of Intralipid plus heparin in rats significantly decreased the insulin dependent-glucose uptake, as well as GLUT4 gene expression in muscular tissue. On the other hand it has been shown that an enhanced plasma lactate concentration may increase insulin secretion and hepatic insulin clearance. Moreover we observed that chronic hyperlactatemia in rats is able to decrease glucose uptake in muscles, while reducing GLUT4 mRNA and protein in the same tissues. In obesity, lactate and FFA overproduction from visceral fat may therefore play a synergic role in reducing insulin sensitivity.</p>","PeriodicalId":14227,"journal":{"name":"International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/sj.ijo.0801271","citationCount":"17","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/sj.ijo.0801271","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 17

Abstract

Increased basal plasma FFA and lactate concentrations are often present in obesity and may deeply affect insulin action. The inhibition of glucose transport or phosphorylation is thought to be involved in this phenomenon, but the molecular mechanisms on the basis are still unknown. In our laboratory we observed that a chronic infusion of Intralipid plus heparin in rats significantly decreased the insulin dependent-glucose uptake, as well as GLUT4 gene expression in muscular tissue. On the other hand it has been shown that an enhanced plasma lactate concentration may increase insulin secretion and hepatic insulin clearance. Moreover we observed that chronic hyperlactatemia in rats is able to decrease glucose uptake in muscles, while reducing GLUT4 mRNA and protein in the same tissues. In obesity, lactate and FFA overproduction from visceral fat may therefore play a synergic role in reducing insulin sensitivity.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
动物模型中的底物竞争和胰岛素作用。
基础血浆游离脂肪酸和乳酸浓度升高常出现在肥胖中,并可能深刻影响胰岛素的作用。葡萄糖转运或磷酸化的抑制被认为参与了这一现象,但其基础的分子机制尚不清楚。在我们的实验室中,我们观察到长期输注脂内加肝素可以显著降低大鼠的胰岛素依赖型葡萄糖摄取,以及肌肉组织中GLUT4基因的表达。另一方面,已证明血浆乳酸浓度的增加可增加胰岛素分泌和肝脏胰岛素清除率。此外,我们观察到大鼠慢性高乳酸血症能够减少肌肉中的葡萄糖摄取,同时减少相同组织中的GLUT4 mRNA和蛋白。在肥胖中,内脏脂肪产生的乳酸和游离脂肪酸过量可能在降低胰岛素敏感性方面发挥协同作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores. Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance. Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1