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成骨细胞中的脂肪酸代谢。

Fatty acid metabolism by the osteoblast.

机构信息

Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Bone. 2018 Oct;115:8-14. doi: 10.1016/j.bone.2017.08.024. Epub 2017 Aug 31.

DOI:10.1016/j.bone.2017.08.024
PMID:28863948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5832496/
Abstract

The emergence of bone as an endocrine organ able to influence whole body metabolism, together with comorbid epidemics of obesity, diabetes, and osteoporosis, have prompted a renewed interest in the intermediary metabolism of the osteoblast. To date, most studies have focused on the utilization of glucose by this specialized cell, but the oxidation of fatty acids results in a larger energy yield. Osteoblasts express the requisite receptors and catabolic enzymes to take up and then metabolize fatty acids, which appears to be required during later stages of differentiation when the osteoblast is dedicated to matrix production and mineralization. In this article, we provide an overview of fatty acid β-oxidation and highlight studies demonstrating that the skeleton plays a significant role in the clearance of circulating lipoproteins and non-esterified fatty acids. Additionally, we review the requirement for long-chain fatty acid metabolism during post-natal bone development and the effects of anabolic stimuli on fatty acid utilization by osteoblasts. These recent findings may help to explain the skeletal manifestations of human diseases associated with impaired lipid metabolism while also providing additional insights into the metabolic requirements of skeletal homeostasis.

摘要

骨骼作为一个能够影响全身代谢的内分泌器官的出现,加上肥胖症、糖尿病和骨质疏松症等共病的流行,促使人们重新关注成骨细胞的中间代谢。迄今为止,大多数研究都集中在这种特殊细胞对葡萄糖的利用上,但脂肪酸的氧化会产生更大的能量产量。成骨细胞表达必要的受体和分解代谢酶来摄取并代谢脂肪酸,这在分化的后期阶段似乎是必需的,此时成骨细胞专门用于基质生成和矿化。本文概述了脂肪酸β氧化,并强调了一些研究表明,骨骼在清除循环脂蛋白和非酯化脂肪酸方面起着重要作用。此外,我们还回顾了长链脂肪酸代谢在出生后骨骼发育中的必要性,以及合成代谢刺激对成骨细胞利用脂肪酸的影响。这些新发现可能有助于解释与脂质代谢受损相关的人类疾病的骨骼表现,同时也为骨骼内稳态的代谢需求提供了更多的见解。

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本文引用的文献

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Fatty acid oxidation by the osteoblast is required for normal bone acquisition in a sex- and diet-dependent manner.成骨细胞进行的脂肪酸氧化以性别和饮食依赖的方式对正常骨量获取是必需的。
JCI Insight. 2017 Aug 17;2(16). doi: 10.1172/jci.insight.92704.
2
Loss of Hepatic Mitochondrial Long-Chain Fatty Acid Oxidation Confers Resistance to Diet-Induced Obesity and Glucose Intolerance.肝脏线粒体长链脂肪酸氧化功能丧失赋予对饮食诱导的肥胖和葡萄糖不耐受的抗性。
Cell Rep. 2017 Jul 18;20(3):655-667. doi: 10.1016/j.celrep.2017.06.080.
3
Quantification of Bone Fatty Acid Metabolism and Its Regulation by Adipocyte Lipoprotein Lipase.骨脂肪酸代谢的定量分析及其受脂肪细胞脂蛋白脂肪酶的调节
Int J Mol Sci. 2017 Jun 13;18(6):1264. doi: 10.3390/ijms18061264.
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Glucagon-induced extracellular cAMP regulates hepatic lipid metabolism.胰高血糖素诱导的细胞外环磷酸腺苷调节肝脏脂质代谢。
J Endocrinol. 2017 Aug;234(2):73-87. doi: 10.1530/JOE-16-0649. Epub 2017 May 17.
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