Peroxisomal 2-Hydroxyacyl-CoA Lyase Is Involved in Endogenous Biosynthesis of Heptadecanoic Acid.
Peroxisomal 2-Hydroxyacyl-CoA Lyase Is Involved in Endogenous Biosynthesis of Heptadecanoic Acid.
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DOI：
10.3390/molecules22101718
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发表时间：
2017-10-13
期刊：
影响因子：
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通讯作者：
Koulman A
中科院分区：
文献类型：
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作者：
Jenkins B;de Schryver E;Van Veldhoven PP;Koulman A
据报道，循环十七烷酸（C17：0）是一种病理风险/预后生物标志物和饮食生物标志物。这种病理学关系已被证明是可靠的预测，即使在独立的饮食贡献，这表明内源性生物合成的C17：0是相关的病理病因。关于C17：0的生物合成，哪些组织有助于循环水平，以及C17：0如何与病理学相关知之甚少。使Hacl 1 +/−小鼠交配以获得Hacl 1 −/−和Hacl 1 +/+对照小鼠。在14周时，它们被麻醉用于组织收集和脂肪酸分析。与Hacl 1 +/+相比，C15：0在任何Hacl 1 −/−组织中均未受到显著影响。然而，Hacl 1 −/−血浆和肝脏C17：0水平显著较低：分别为~26%和~ 22%。在不同脂肪组织中未观察到显著差异。总之，Hacl 1在肝脏和血浆C17：0水平中起着重要作用，这提供了它可以通过α-氧化内源性生物合成的证据。C17：0与病理学的强烈负相关性提出了α-氧化与这些疾病之间是否存在直接联系的问题。目前，还没有明确的证据，阻碍了进一步研究α-氧化在代谢性疾病中的作用。
Circulating heptadecanoic acid (C17:0) is reported to be a pathology risk/prognosis biomarker and a dietary biomarker. This pathology relationship has been shown to be reliably predictive even when independent of dietary contributions, suggesting that the endogenous biosynthesis of C17:0 is related to the pathological aetiology. Little is known about C17:0 biosynthesis, which tissues contribute to the circulating levels, and how C17:0 is related to pathology. Hacl1+/− mice were mated to obtain Hacl1−/− and Hacl1+/+ control mice. At 14 weeks, they were anesthetized for tissue collection and fatty acid analysis. Compared to Hacl1+/+, C15:0 was not significantly affected in any Hacl1−/− tissues. However, the Hacl1−/− plasma and liver C17:0 levels were significantly lower: ~26% and ~22%, respectively. No significant differences were seen in the different adipose tissues. To conclude, Hacl1 plays a significant role in the liver and plasma levels of C17:0, providing evidence it can be endogenously biosynthesized via alpha-oxidation. The strong inverse association of C17:0 with pathology raises the question whether there is a direct link between α-oxidation and these diseases. Currently, there is no clear evidence, warranting further research into the role of α-oxidation in relation to metabolic diseases.