• 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

胰岛素可在体内急性上调人体骨骼肌中脂肪酸转运蛋白CD36的蛋白表达。

Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo.

作者信息

Corpeleijn E, Pelsers M M A L, Soenen S, Mensink M, Bouwman F G, Kooi M E, Saris W H M, Glatz J F C, Blaak E E

机构信息

From the Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

出版信息

J Physiol Pharmacol. 2008 Mar;59(1):77-83.

PMID:18441389
Abstract

Enhanced fatty acid uptake may lead to the accumulation of lipid intermediates. This is related to insulin resistance and type 2 diabetes mellitus. Rodent studies suggest that fatty acid transporters are acutely regulated by insulin. We investigated differences in fatty acid transporter content before and at the end of a hyperinsulinemic euglycemic clamp in skeletal muscle (m. vastus lateralis) of obese, glucose-intolerant men (IGT) and obese normal glucose tolerant controls (NGT). The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. No change was seen in cytosolic fatty acid binding protein (FABPc) protein content. The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). An increase in FAT/CD36 protein content in skeletal muscle may result in a higher fractional extraction of fatty acids (larger relative uptake) after a meal, enhancing triglyceride accumulation in the muscle. We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term.

摘要

脂肪酸摄取增加可能导致脂质中间体的积累。这与胰岛素抵抗和2型糖尿病有关。啮齿动物研究表明,脂肪酸转运蛋白受胰岛素急性调节。我们调查了肥胖、糖耐量受损男性(IGT)和肥胖糖耐量正常对照组(NGT)的骨骼肌(股外侧肌)在高胰岛素正常血糖钳夹试验开始前和结束时脂肪酸转运蛋白含量的差异。胰岛素刺激3小时后,脂肪酸转运蛋白FAT/CD36的蛋白质含量增加了1.5倍(P<0.05),IGT组和对照组之间无差异。胞质脂肪酸结合蛋白(FABPc)的蛋白质含量未见变化。FAT/CD36蛋白质含量的增加与钳夹试验期间测得的胰岛素抵抗呈正相关(r=0.56,P<0.05)。骨骼肌中FAT/CD36蛋白质含量的增加可能导致餐后脂肪酸的更高分数提取(更大的相对摄取),从而增强肌肉中甘油三酯的积累。我们得出结论,在肥胖人群中,骨骼肌中的FAT/CD36蛋白质含量在体内短期内也受胰岛素的动态调节。

相似文献

1
Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo.胰岛素可在体内急性上调人体骨骼肌中脂肪酸转运蛋白CD36的蛋白表达。
J Physiol Pharmacol. 2008 Mar;59(1):77-83.
2
The fatty acid transporter FAT/CD36 is upregulated in subcutaneous and visceral adipose tissues in human obesity and type 2 diabetes.脂肪酸转运蛋白FAT/CD36在人类肥胖症和2型糖尿病患者的皮下及内脏脂肪组织中表达上调。
Int J Obes (Lond). 2006 Jun;30(6):877-83. doi: 10.1038/sj.ijo.0803212.
3
Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36.人类肥胖和2型糖尿病中的三酰甘油蓄积与骨骼肌脂肪酸转运速率增加以及肌膜脂肪酸转运蛋白/分化簇36(FAT/CD36)增加有关。
FASEB J. 2004 Jul;18(10):1144-6. doi: 10.1096/fj.03-1065fje. Epub 2004 May 7.
4
Fatty acid transport and FAT/CD36 are increased in red but not in white skeletal muscle of ZDF rats.脂肪酸转运及FAT/CD36在ZDF大鼠的红色骨骼肌中增加,但在白色骨骼肌中未增加。
Am J Physiol Endocrinol Metab. 2006 Sep;291(3):E675-82. doi: 10.1152/ajpendo.00096.2006. Epub 2006 May 9.
5
Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects.噻唑烷二酮类药物可上调2型糖尿病患者骨骼肌中受损的脂肪酸摄取。
Am J Physiol Endocrinol Metab. 2003 Aug;285(2):E354-62. doi: 10.1152/ajpendo.00491.2001. Epub 2003 Apr 15.
6
Skeletal muscle mitochondrial FAT/CD36 content and palmitate oxidation are not decreased in obese women.肥胖女性的骨骼肌线粒体FAT/CD36含量和棕榈酸氧化并未降低。
Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1782-9. doi: 10.1152/ajpendo.00639.2006. Epub 2007 Feb 20.
7
Impaired skeletal muscle substrate oxidation in glucose-intolerant men improves after weight loss.糖耐量受损男性减重后骨骼肌底物氧化功能改善。
Obesity (Silver Spring). 2008 May;16(5):1025-32. doi: 10.1038/oby.2008.24. Epub 2008 Feb 28.
8
A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism.骨骼肌中FAT/CD36的无效突变揭示了其在胰岛素和AICAR刺激的脂肪酸代谢中的重要作用。
Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1740-9. doi: 10.1152/ajpendo.00579.2006. Epub 2007 Jan 30.
9
Effect of a 2-day very low-energy diet on skeletal muscle insulin sensitivity in obese type 2 diabetic patients on insulin therapy.为期2天的极低能量饮食对接受胰岛素治疗的肥胖2型糖尿病患者骨骼肌胰岛素敏感性的影响。
Metabolism. 2005 Dec;54(12):1669-78. doi: 10.1016/j.metabol.2005.06.017.
10
Insulin stimulates fatty acid transport by regulating expression of FAT/CD36 but not FABPpm.胰岛素通过调节脂肪酸转运蛋白/脂肪酸转位酶(FAT/CD36)的表达来刺激脂肪酸转运,而不是通过调节微粒体脂肪酸结合蛋白(FABPpm)的表达。
Am J Physiol Endocrinol Metab. 2004 Oct;287(4):E781-9. doi: 10.1152/ajpendo.00573.2003. Epub 2004 May 27.

引用本文的文献

1
FAT/CD36 Participation in Human Skeletal Muscle Lipid Metabolism: A Systematic Review.FAT/CD36在人类骨骼肌脂质代谢中的作用:一项系统评价。
J Clin Med. 2022 Dec 31;12(1):318. doi: 10.3390/jcm12010318.
2
Increased plasma fatty acid clearance, not fatty acid concentration, is associated with muscle insulin resistance in people with obesity.肥胖人群中,肌肉胰岛素抵抗与血浆脂肪酸清除率增加有关,而非与脂肪酸浓度有关。
Metabolism. 2022 Jul;132:155216. doi: 10.1016/j.metabol.2022.155216. Epub 2022 May 13.
3
CD 36: Focus on Epigenetic and Post-Transcriptional Regulation.
CD 36:聚焦表观遗传和转录后调控。
Front Genet. 2019 Jul 19;10:680. doi: 10.3389/fgene.2019.00680. eCollection 2019.
4
Bariatric surgery reduces CD36-bearing microvesicles of endothelial and monocyte origin.减肥手术可减少内皮细胞和单核细胞来源的携带CD36的微泡。
Nutr Metab (Lond). 2018 Oct 23;15:76. doi: 10.1186/s12986-018-0309-4. eCollection 2018.
5
Ectopic Fat Accumulation in Distinct Insulin Resistant Phenotypes; Targets for Personalized Nutritional Interventions.不同胰岛素抵抗表型中的异位脂肪堆积;个性化营养干预的靶点
Front Nutr. 2018 Sep 4;5:77. doi: 10.3389/fnut.2018.00077. eCollection 2018.
6
Hyperinsulinemia Enhances Hepatic Expression of the Fatty Acid Transporter Cd36 and Provokes Hepatosteatosis and Hepatic Insulin Resistance.高胰岛素血症增强脂肪酸转运蛋白Cd36的肝脏表达并引发肝脂肪变性和肝脏胰岛素抵抗。
J Biol Chem. 2015 Jul 31;290(31):19034-43. doi: 10.1074/jbc.M115.640292. Epub 2015 Jun 17.
7
Pathways of polyunsaturated fatty acid utilization: implications for brain function in neuropsychiatric health and disease.多不饱和脂肪酸的利用途径:对神经精神健康与疾病中脑功能的影响
Brain Res. 2015 Feb 9;1597:220-46. doi: 10.1016/j.brainres.2014.11.059. Epub 2014 Dec 8.
8
Hyperinsulinemia and skeletal muscle fatty acid trafficking.高胰岛素血症与骨骼肌脂肪酸转运。
Am J Physiol Endocrinol Metab. 2013 Aug 15;305(4):E540-8. doi: 10.1152/ajpendo.00143.2013. Epub 2013 Jul 2.
9
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice.循环胰岛素通过中枢神经系统 KATP 通道激活仅在胰岛素敏感的小鼠中刺激白色脂肪组织中脂肪酸的保留。
J Lipid Res. 2011 Sep;52(9):1712-22. doi: 10.1194/jlr.M015396. Epub 2011 Jun 23.
10
The role of mitochondria in the pathophysiology of skeletal muscle insulin resistance.线粒体在骨骼肌胰岛素抵抗的病理生理学中的作用。
Endocr Rev. 2010 Feb;31(1):25-51. doi: 10.1210/er.2009-0003. Epub 2009 Oct 27.