CrossTalk opposing view: Intramyocellular ceramide accumulation does not modulate insulin resistance.
CrossTalk opposing view: Intramyocellular ceramide accumulation does not modulate insulin resistance.
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CrossTalk 相反的观点：肌细胞内神经酰胺的积累不会调节胰岛素抵抗。
DOI：
10.1113/jp271677
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Jurczak,MichaelJ
中科院分区：
文献类型：
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作者：
Petersen,MaxC;Jurczak,MichaelJ
脂质代谢失调导致肌肉胰岛素抵抗的假说已经有半个多世纪的历史（Randle et al. 1963）。尽管早期的研究表明葡萄糖和脂肪氧化的相互变构调节是脂质诱导的葡萄糖代谢损伤的机制（Randle et al. 1963），但最近的研究表明，具有信号传导特性的不同脂质物质直接干扰胰岛素信号传导级联反应，产生胰岛素抵抗（Shulman，2014）。早期的研究表明细胞内神经酰胺水平和胰岛素抵抗之间的关系是在细胞培养中进行的;向培养基中加入棕榈酸酯或细胞渗透性短链神经酰胺，通常在超生理浓度下，反复显示会损害胰岛素作用（Summers等人，2005）。
The hypothesis that dysregulated lipid metabolism contributes to insulin resistance in muscle is now over a half-century old (Randle et al. 1963). Although early work implicated reciprocal allosteric regulation of glucose and fat oxidation as a mechanism for lipid-induced impairments in glucose metabolism (Randle et al. 1963), more recent studies propose that distinct lipid species with signalling properties directly interfere with the insulin signalling cascade to produce insulin resistance (Shulman, 2014). Of the many lipid metabolites proposed to cause insulin resistance, the ceramides have received particular attention.Early studies demonstrating a relationship between intracellular ceramide levels and insulin resistance were performed in cell culture; the addition of palmitate or cellpermeant short-chain ceramides to the culture medium, often at supraphysiological concentrations, was repeatedly shown to impair insulin action (Summers et al.