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Excess exposure to insulin may be the primary cause of insulin resistance.

作者信息

Cao Wenhong, Liu Hui-Yu, Hong Tao, Liu Zhenqi

出版信息

Am J Physiol Endocrinol Metab. 2010 Feb;298(2):E372. doi: 10.1152/ajpendo.00677.2009.

DOI:10.1152/ajpendo.00677.2009
PMID:20075432
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2822476/
Abstract
摘要

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1
Excess exposure to insulin may be the primary cause of insulin resistance.胰岛素暴露过多可能是胰岛素抵抗的主要原因。
Am J Physiol Endocrinol Metab. 2010 Feb;298(2):E372. doi: 10.1152/ajpendo.00677.2009.
2
[Hepatic insulin resistance and energy homeostasis].[肝脏胰岛素抵抗与能量稳态]
Nihon Rinsho. 2006 Dec 28;64 Suppl 9:145-8.
3
[Insulin resistance and atherosclerosis].[胰岛素抵抗与动脉粥样硬化]
Acta Med Port. 2000 Jul-Aug;13(4):203-10.
4
Insulin resistance and hypertension--implications for treatment.胰岛素抵抗与高血压——治疗的意义
Postgrad Med J. 1991 Oct;67(792):869-75. doi: 10.1136/pgmj.67.792.869.
5
Insulin-Mediated Diseases: Adrenal Mass and Polycystic Ovary Syndrome.胰岛素介导疾病:肾上腺肿块和多囊卵巢综合征。
Trends Endocrinol Metab. 2015 Oct;26(10):512-514. doi: 10.1016/j.tem.2015.07.010.
6
Syndrome X: a cause of hypertension? Negative.X综合征:高血压的一个病因?否定。
Hosp Pract (Off Ed). 1992 Feb;27 Suppl 1:41-4; discussion 44-5.
7
Insulin resistance, energy balance and sympathetic nervous system activity.胰岛素抵抗、能量平衡与交感神经系统活动。
Clin Exp Hypertens A. 1990;12(5):817-30. doi: 10.3109/10641969009073502.
8
Diabetes: have we got it all wrong? Hyperinsulinism as the culprit: surgery provides the evidence.糖尿病:我们是否完全搞错了?高胰岛素血症才是罪魁祸首:手术提供了证据。
Diabetes Care. 2012 Dec;35(12):2438-42. doi: 10.2337/dc12-0684.
9
[Hyperinsulinism/insulin resistance: cause, effect or marker of essential arterial hypertension?].[高胰岛素血症/胰岛素抵抗:原发性动脉高血压的原因、结果还是标志物?]
G Ital Cardiol. 1995 Feb;25(2):207-16.
10
IL-6 and metabolism-new evidence and new questions.白细胞介素-6与代谢——新证据与新问题
Diabetologia. 2008 Jul;51(7):1097-9. doi: 10.1007/s00125-008-1019-7.

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In Vitro Chronic Hyperinsulinemia Induces Remodelling of Vascular Smooth Muscle Cells from Young Men and Women in a Sex Hormone Independent Manner.体外慢性高胰岛素血症以性激素非依赖性方式诱导青年男性和女性血管平滑肌细胞重塑。
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Overnutrition, Hyperinsulinemia and Ectopic Fat: It Is Time for A Paradigm Shift in the Management of Type 2 Diabetes.营养过剩、高胰岛素血症和异位脂肪:是时候改变 2 型糖尿病的治疗模式了。
Int J Mol Sci. 2024 May 17;25(10):5488. doi: 10.3390/ijms25105488.
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Low Carbohydrate Dietary Approaches for People With Type 2 Diabetes-A Narrative Review.2型糖尿病患者的低碳水化合物饮食方法——叙述性综述
Front Nutr. 2021 Jul 15;8:687658. doi: 10.3389/fnut.2021.687658. eCollection 2021.
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Optimizing Adult Protein Intake During Catabolic Health Conditions.优化代谢性健康状况下成人的蛋白质摄入量。
Adv Nutr. 2020 Jul 1;11(4):S1058-S1069. doi: 10.1093/advances/nmaa047.
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Targeting insulin to the liver corrects defects in glucose metabolism caused by peripheral insulin delivery.将胰岛素靶向肝脏可以纠正由于外周胰岛素输送引起的葡萄糖代谢缺陷。
JCI Insight. 2019 Feb 26;5(7):126974. doi: 10.1172/jci.insight.126974.
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Effects of dietary fat subtypes on glucose homeostasis during pregnancy in rats.膳食脂肪亚型对大鼠孕期葡萄糖稳态的影响。
Nutr Metab (Lond). 2016 Aug 24;13(1):58. doi: 10.1186/s12986-016-0117-7. eCollection 2016.
7
Changes in glucose and fat metabolism in response to the administration of a hepato-preferential insulin analog.给予肝脏优先作用胰岛素类似物后葡萄糖和脂肪代谢的变化
Diabetes. 2014 Nov;63(11):3946-54. doi: 10.2337/db14-0266. Epub 2014 Jun 19.
8
Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms.胰岛素信号转导、抵抗与代谢综合征:疾病机制的小鼠模型研究进展。
J Endocrinol. 2014 Jan 8;220(2):T1-T23. doi: 10.1530/JOE-13-0327. Print 2014 Feb.
9
Myocardial loss of IRS1 and IRS2 causes heart failure and is controlled by p38α MAPK during insulin resistance.IRS1 和 IRS2 在心肌中的缺失会导致心力衰竭,并且在胰岛素抵抗期间受 p38α MAPK 调控。
Diabetes. 2013 Nov;62(11):3887-900. doi: 10.2337/db13-0095.
10
The pancreas is altered by in utero androgen exposure: implications for clinical conditions such as polycystic ovary syndrome (PCOS).子宫内雄激素暴露会改变胰腺:这对多囊卵巢综合征(PCOS)等临床情况有影响。
PLoS One. 2013;8(2):e56263. doi: 10.1371/journal.pone.0056263. Epub 2013 Feb 15.

本文引用的文献

1
Hepatic autophagy is suppressed in the presence of insulin resistance and hyperinsulinemia: inhibition of FoxO1-dependent expression of key autophagy genes by insulin.在存在胰岛素抵抗和高胰岛素血症的情况下,肝脏自噬受到抑制:胰岛素抑制关键自噬基因的FoxO1依赖性表达。
J Biol Chem. 2009 Nov 6;284(45):31484-92. doi: 10.1074/jbc.M109.033936. Epub 2009 Sep 16.
2
Insulin is a stronger inducer of insulin resistance than hyperglycemia in mice with type 1 diabetes mellitus (T1DM).在1型糖尿病(T1DM)小鼠中,胰岛素比高血糖更易诱导胰岛素抵抗。
J Biol Chem. 2009 Oct 2;284(40):27090-100. doi: 10.1074/jbc.M109.016675. Epub 2009 Aug 4.
3
Increased basal level of Akt-dependent insulin signaling may be responsible for the development of insulin resistance.胰岛素信号通路中 Akt 依赖性基础水平的增加可能是导致胰岛素抵抗发生的原因。
Am J Physiol Endocrinol Metab. 2009 Oct;297(4):E898-906. doi: 10.1152/ajpendo.00374.2009. Epub 2009 Jul 28.
4
Prolonged exposure to insulin suppresses mitochondrial production in primary hepatocytes.长期暴露于胰岛素会抑制原代肝细胞中的线粒体生成。
J Biol Chem. 2009 May 22;284(21):14087-95. doi: 10.1074/jbc.M807992200. Epub 2009 Mar 31.
5
The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit.四氧嘧啶糖尿病对家兔实验性胆固醇动脉粥样硬化的影响。
J Exp Med. 1949 Jun 1;89(6):611-30. doi: 10.1084/jem.89.6.611.
6
The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. III. The mechanism of the inhibition of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits.四氧嘧啶糖尿病对家兔实验性胆固醇动脉粥样硬化的影响。III. 四氧嘧啶糖尿病家兔实验性胆固醇动脉粥样硬化抑制机制
J Exp Med. 1950 Oct 1;92(4):299-317. doi: 10.1084/jem.92.4.299.
7
Effect of insulin in the induction and regression of atherosclerosis in the chick.胰岛素对雏鸡动脉粥样硬化诱导和消退的作用。
Circ Res. 1960 May;8:572-6. doi: 10.1161/01.res.8.3.572.
8
The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. IV. The effect of insulin therapy on the inhibition of atherosclerosis in the alloxan-diabetic rabbit.四氧嘧啶糖尿病对家兔实验性胆固醇动脉粥样硬化的影响。IV. 胰岛素治疗对四氧嘧啶糖尿病家兔动脉粥样硬化抑制作用的影响。
J Exp Med. 1954 Oct 1;100(4):371-80. doi: 10.1084/jem.100.4.371.
9
The mechanism of alloxan protection in experimental atherosclerosis.四氧嘧啶在实验性动脉粥样硬化中的保护机制。
J Exp Med. 1954 Feb;99(2):119-24. doi: 10.1084/jem.99.2.119.