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首页> 外文期刊>Islets >Palmitate is not an effective fuel for pancreatic islets and amplifies insulin secretion independent of calcium release from endoplasmic reticulum
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Palmitate is not an effective fuel for pancreatic islets and amplifies insulin secretion independent of calcium release from endoplasmic reticulum

机译：棕榈酸不是胰岛素的有效燃料，并与内质网的钙释放无关放大胰岛素分泌物

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The aim of the study was to determine the acute contribution of fuel oxidation in mediating the increase in insulin secretion rate (ISR) in response to fatty acids. Measures of mitochondrial metabolism, as reflected by oxygen consumption rate (OCR) and cytochrome c reduction, calcium signaling, and ISR by rat islets were used to evaluate processes stimulated by acute exposure to palmitic acid (PA). The contribution of mitochondrial oxidation of PA was determined in the presence and absence of a blocker of mitochondrial transport of fatty acids (etomoxir) at different glucose concentrations. Subsequent to increasing glucose from 3 to 20 mM, PA caused small increases in OCR and cytosolic calcium (about 20% of the effect of glucose). In contrast, the effect of PA on ISR was almost 3 times that by glucose, suggesting that the metabolism of PA is not the dominant mechanism mediating PA's effect on ISR. This was further supported by lack of inhibition of PA-stimulated OCR and ISR when blocking entry of PA into mitochondria (with etomoxir), and PA's lack of stimulation of reduced cytochrome c in the presence of high glucose. Consistent with the lack of metabolic stimulation by PA, an inhibitor of calcium release from the endoplasmic reticulum, but not a blocker of L-type calcium channels, abolished the PA-induced elevation of cytosolic calcium. Notably, ISR was unaffected by thapsigargin showing the dissociation of endoplasmic reticulum calcium release and second phase insulin secretion. In conclusion, stimulation of ISR by PA was mediated by mechanisms largely independent of the oxidation of the fuel.
机译：该研究的目的是确定燃料氧化在介于脂肪酸响应胰岛素分泌率（ISR）的增加时急性贡献。用氧消耗率（OCR）和细胞色素C还原，钙信号传导和大鼠胰岛的含量的线粒体代谢测量用于评估急性暴露于棕榈酸（PA）刺激刺激的方法。在不同葡萄糖浓度下在不同葡萄糖浓度下的脂肪酸（Etomoxir）的线粒体传输的阻塞中确定了Pa的线粒体氧化的贡献。在将葡萄糖增加3至20mm后，PA引起了OCR和胞质溶解的小增加（葡萄糖效果的约20％）。相比之下，PA对ISR的影响几乎是葡萄糖的3倍，表明PA的代谢不是调解PA对ISR影响的主导机制。通过缺乏对PA刺激的OCR和ISR的抑制进一步支持这一点，当阻止PA进入线粒体（用Etomoxir），并且PA在高葡萄糖存在下缺乏刺激细胞色素C.通过PA的缺乏代谢刺激，从内质网的钙释放抑制剂，但不是L型钙通道的阻断剂，废除了PA诱导的细胞溶质钙的升高。值得注意的是，ISR不受Thapsigargin的影响，显示出内质网钙释放和第二阶段胰岛素分泌的解离。总之，PA通过PA的ISR刺激通过大量独立于燃料氧化的机制介导。

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