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本文引用的文献

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mTOR: from growth signal integration to cancer, diabetes and ageing.mTOR:从生长信号整合到癌症、糖尿病和衰老。
Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35. doi: 10.1038/nrm3025. Epub 2010 Dec 15.
2
mTOR attenuates the inflammatory response in cardiomyocytes and prevents cardiac dysfunction in pathological hypertrophy.雷帕霉素靶蛋白(mTOR)可减弱心肌细胞中的炎症反应,防止病理性心肌肥厚导致的心脏功能障碍。
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MTORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice.雷帕霉素靶蛋白复合物 1 通过抑制 4E-BP1 调节心脏功能和心肌细胞存活。
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4
Mitochondria in the diabetic heart.糖尿病心脏中的线粒体。
Cardiovasc Res. 2010 Nov 1;88(2):229-40. doi: 10.1093/cvr/cvq239. Epub 2010 Jul 16.
5
Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance.长时间禁食将骨骼肌线粒体功能障碍确定为人类胰岛素抵抗的结果而非原因。
Diabetes. 2010 Sep;59(9):2117-25. doi: 10.2337/db10-0519. Epub 2010 Jun 23.
6
Muscle insulin resistance: assault by lipids, cytokines and local macrophages.肌肉胰岛素抵抗:脂质、细胞因子和局部巨噬细胞的攻击。
Curr Opin Clin Nutr Metab Care. 2010 Jul;13(4):382-90. doi: 10.1097/MCO.0b013e32833aabd9.
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Cardiac and metabolic changes in long-term high fructose-fat fed rats with severe obesity and extensive intramyocardial lipid accumulation.长期高果糖高脂肪喂养致严重肥胖和广泛心肌内脂质蓄积大鼠的心脏和代谢变化。
Am J Physiol Regul Integr Comp Physiol. 2010 Jun;298(6):R1560-70. doi: 10.1152/ajpregu.00392.2009. Epub 2010 Mar 31.
8
Fat cell-specific ablation of rictor in mice impairs insulin-regulated fat cell and whole-body glucose and lipid metabolism.脂肪细胞特异性敲除小鼠中的rictor 会损害胰岛素调节的脂肪细胞和全身葡萄糖及脂质代谢。
Diabetes. 2010 Jun;59(6):1397-406. doi: 10.2337/db09-1061. Epub 2010 Mar 23.
9
Macrophages, inflammation, and insulin resistance.巨噬细胞、炎症与胰岛素抵抗。
Annu Rev Physiol. 2010;72:219-46. doi: 10.1146/annurev-physiol-021909-135846.
10
Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1.JNK1 在代谢调节中的作用:下丘脑-垂体-甲状腺轴。
Genes Dev. 2010 Feb 1;24(3):256-64. doi: 10.1101/gad.1878510. Epub 2010 Jan 15.

糖尿病心脏中胰岛素抵抗的新见解。

New insights into insulin resistance in the diabetic heart.

机构信息

Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

出版信息

Trends Endocrinol Metab. 2011 Oct;22(10):394-403. doi: 10.1016/j.tem.2011.05.001. Epub 2011 Jun 15.

DOI:10.1016/j.tem.2011.05.001
PMID:21680199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3183400/
Abstract

Insulin resistance is a major characteristic of obesity and type 2 diabetes, and develops in multiple organs, including the heart. Compared with its role in other organs, the physiological role of insulin resistance in the heart is not well understood. The heart uses lipid as a primary fuel, but glucose becomes an important source of energy in ischemia. The impaired ability to utilize glucose might contribute to cell death and abnormal function in the diabetic heart. Recent discoveries regarding the role of inflammation, mitochondrial dysfunction and endoplasmic reticulum (ER) stress in obesity have advanced our understanding of how insulin resistance develops in peripheral organs. In this review, we examine these findings in relation to the diabetic heart to provide new insights into the mechanism of cardiac insulin resistance.

摘要

胰岛素抵抗是肥胖和 2 型糖尿病的主要特征,可发生在多个器官,包括心脏。与在其他器官中的作用相比,胰岛素抵抗在心脏中的生理作用尚不清楚。心脏以脂质作为主要燃料,但在缺血时葡萄糖成为重要的能量来源。葡萄糖利用能力受损可能导致糖尿病心脏中的细胞死亡和功能异常。最近关于炎症、线粒体功能障碍和内质网(ER)应激在肥胖中的作用的发现,促进了我们对周围器官中胰岛素抵抗发展的理解。在这篇综述中,我们研究了这些发现与糖尿病心脏的关系,以期为心脏胰岛素抵抗的机制提供新的见解。