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营养感知与利用:探寻代谢灵活性的核心

Nutrient sensing and utilization: Getting to the heart of metabolic flexibility.

作者信息

Griffin Timothy M, Humphries Kenneth M, Kinter Michael, Lim Hui-Ying, Szweda Luke I

机构信息

Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA; Department of Geriatric Medicine, Reynolds Oklahoma Center on Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA; Department of Geriatric Medicine, Reynolds Oklahoma Center on Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

出版信息

Biochimie. 2016 May;124:74-83. doi: 10.1016/j.biochi.2015.10.013. Epub 2015 Oct 22.

DOI:10.1016/j.biochi.2015.10.013
PMID:26476002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4828282/
Abstract

A central feature of obesity-related cardiometabolic diseases is the impaired ability to transition between fatty acid and glucose metabolism. This impairment, referred to as "metabolic inflexibility", occurs in a number of tissues, including the heart. Although the heart normally prefers to metabolize fatty acids over glucose, the inability to upregulate glucose metabolism under energetically demanding conditions contributes to a pathological state involving energy imbalance, impaired contractility, and post-translational protein modifications. This review discusses pathophysiologic processes that contribute to cardiac metabolic inflexibility and speculates on the potential physiologic origins that lead to the current state of cardiometabolic disease in an obesogenic environment.

摘要

肥胖相关的心脏代谢疾病的一个核心特征是脂肪酸和葡萄糖代谢之间转换能力受损。这种损害,即所谓的“代谢灵活性受损”,发生在包括心脏在内的许多组织中。尽管心脏通常更喜欢代谢脂肪酸而非葡萄糖,但在能量需求较高的情况下无法上调葡萄糖代谢会导致一种涉及能量失衡、收缩功能受损和翻译后蛋白质修饰的病理状态。本综述讨论了导致心脏代谢灵活性受损的病理生理过程,并推测了在致肥胖环境中导致当前心脏代谢疾病状态的潜在生理根源。

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本文引用的文献

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Immune regulation of metabolic homeostasis in health and disease.健康与疾病状态下代谢稳态的免疫调节
Cell. 2015 Mar 26;161(1):146-160. doi: 10.1016/j.cell.2015.02.022.
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Tipping the metabolic scales towards increased longevity in mammals.促使哺乳动物代谢平衡向延长寿命方向倾斜。
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Diabetes and cardiac autonomic neuropathy: Clinical manifestations, cardiovascular consequences, diagnosis and treatment.糖尿病与心脏自主神经病变:临床表现、心血管后果、诊断与治疗。
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Metabolic inflexibility: when mitochondrial indecision leads to metabolic gridlock.代谢灵活性受损:线粒体决策失误导致代谢僵局。
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MED13-dependent signaling from the heart confers leanness by enhancing metabolism in adipose tissue and liver.心脏中MED13依赖的信号传导通过增强脂肪组织和肝脏的代谢赋予瘦体型。
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Adiponectin stimulates Rho-mediated actin cytoskeleton remodeling and glucose uptake via APPL1 in primary cardiomyocytes.脂联素通过 APPL1 刺激原代心肌细胞中的 Rho 介导的肌动蛋白细胞骨架重塑和葡萄糖摄取。
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The growing landscape of lysine acetylation links metabolism and cell signalling.赖氨酸乙酰化修饰将代谢与细胞信号联系起来的研究现状。
Nat Rev Mol Cell Biol. 2014 Aug;15(8):536-50. doi: 10.1038/nrm3841.
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Rescue of cardiac leptin receptors in db/db mice prevents myocardial triglyceride accumulation.拯救db/db小鼠的心脏瘦素受体可防止心肌甘油三酯积聚。
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