The current study aims to evaluate whether peripheral blood miR-324-5p could be used to differentiate patients with metabolic disorders and healthy controls. Our data showed that miR-324-5p levels were elevated in the peripheral blood of patients with hyperglycemia or hyperlipidemia. In addition, the expression of miR-324-5p was enhanced in the peripheral blood and liver of db/db mice. Further study indicated that overexpression of miR-324-5p reduced the activation of the AKT/GSK pathway and increased lipid accumulation, while the inhibition of miR-324-5p activated the AKT/GSK pathway and decreased lipid accumulation. A dual luciferase assay revealed that Rho-associated coiled-coil containing protein kinase 1 (ROCK1) was a target gene of miR-324-5p. In addition, silencing ROCK1 deteriorated lipid and glucose metabolism. More importantly, knockdown of ROCK1 reversed the miR-324-5p inhibitor-induced improvement of glucose and lipid metabolism. In summary, miR-324-5p plays a regulatory role in glucose and lipid metabolism by targeting ROCK1, which is involved in metabolic disorders. The use of miR-324-5p in diagnosing metabolic syndrome is worth investigating and may benefit patients.

中文翻译：

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通过抑制ROCK1，增强的外周血miR-324-5p与代谢综合征的风险相关。

本研究旨在评估外周血miR-324-5p是否可用于区分代谢异常患者和健康对照者。我们的数据显示，高血糖或高血脂患者的外周血中miR-324-5p水平升高。此外，在db / db小鼠的外周血和肝脏中，miR-324-5p的表达增强。进一步的研究表明，miR-324-5p的过表达减少了AKT / GSK途径的激活并增加了脂质的积累，而对miR-324-5p的抑制则激活了AKT / GSK途径并减少了脂质的积累。双重荧光素酶测定法显示，含有Rho的含有蛋白激酶1（ROCK1）的卷曲螺旋是miR-324-5p的靶基因。另外，沉默ROCK1使脂质和葡萄糖代谢恶化。更重要的是，敲低ROCK1可逆转miR-324-5p抑制剂诱导的葡萄糖和脂质代谢改善。总之，miR-324-5p通过靶向参与代谢异常的ROCK1在葡萄糖和脂质代谢中发挥调节作用。miR-324-5p在诊断代谢综合征中的用途值得研究，可能会使患者受益。