Abstract：
BACKGROUND: Both hyperuricaemia and hyperlipidaemia are common metabolic diseases that are closely related to each other, and both are independent risk factors for the development of a variety of diseases. HUA combined with hyperlipidaemia increases the risk of nonalcoholic fatty liver disease and coronary heart disease. This study aimed to investigate the relationship between HUA and hyperlipidaemia and study the metabolic pathway changes in patients with HUA associated with hyperlipidaemia using metabolomics.
METHODS: This was a case‒control study. The prevalence of hyperlipidaemia in HUA patients in the physical examination population of Tianjin Union Medical Centre in 2018 was investigated. Metabolomics analysis was performed on 308 HUA patients and 100 normal controls using Orbitrap mass spectrometry. A further metabolomics study of 30 asymptomatic HUA patients, 30 HUA patients with hyperlipidaemia, and 30 age-and sex-matched healthy controls was conducted. Differential metabolites were obtained from the three groups by orthogonal partial least-squares discrimination analysis, and relevant metabolic pathways changes were analysed using MetaboAnalyst 5.0 software.
RESULTS: The prevalence of hyperlipidaemia in HUA patients was 69.3%. Metabolomic analysis found that compared with the control group, 33 differential metabolites, including arachidonic acid, alanine, aspartate, phenylalanine and tyrosine, were identified in asymptomatic HUA patients. Pathway analysis showed that these changes were mainly related to 3 metabolic pathways, including the alanine, aspartate and glutamate metabolism pathway. Thirty-eight differential metabolites, including linoleic acid, serine, glutamate, and tyrosine, were identified in HUA patients with hyperlipidaemia. Pathway analysis showed that they were mainly related to 7 metabolic pathways, including the linoleic acid metabolism pathway, phenylalanine, tyrosine and tryptophan biosynthesis pathway, and glycine, serine and threonine metabolism pathway.
CONCLUSIONS: Compared to the general population, the HUA population had a higher incidence of hyperlipidaemia. HUA can cause hyperlipidaemia. by affecting the metabolic pathways of linoleic acid metabolism and alanine, aspartate and glutamate metabolism. Fatty liver is closely associated with changes in the biosynthesis pathway of pahenylalanine, tyrosine, and tryptophan in HUA patients with hyperlipidaemia. Changes in the glycine, serine and threonine metabolism pathway in HUA patients with hyperlipidaemia may lead to chronic kidney disease.
METHODS: This was a case‒control study. The prevalence of hyperlipidaemia in HUA patients in the physical examination population of Tianjin Union Medical Centre in 2018 was investigated. Metabolomics analysis was performed on 308 HUA patients and 100 normal controls using Orbitrap mass spectrometry. A further metabolomics study of 30 asymptomatic HUA patients, 30 HUA patients with hyperlipidaemia, and 30 age-and sex-matched healthy controls was conducted. Differential metabolites were obtained from the three groups by orthogonal partial least-squares discrimination analysis, and relevant metabolic pathways changes were analysed using MetaboAnalyst 5.0 software.
RESULTS: The prevalence of hyperlipidaemia in HUA patients was 69.3%. Metabolomic analysis found that compared with the control group, 33 differential metabolites, including arachidonic acid, alanine, aspartate, phenylalanine and tyrosine, were identified in asymptomatic HUA patients. Pathway analysis showed that these changes were mainly related to 3 metabolic pathways, including the alanine, aspartate and glutamate metabolism pathway. Thirty-eight differential metabolites, including linoleic acid, serine, glutamate, and tyrosine, were identified in HUA patients with hyperlipidaemia. Pathway analysis showed that they were mainly related to 7 metabolic pathways, including the linoleic acid metabolism pathway, phenylalanine, tyrosine and tryptophan biosynthesis pathway, and glycine, serine and threonine metabolism pathway.
CONCLUSIONS: Compared to the general population, the HUA population had a higher incidence of hyperlipidaemia. HUA can cause hyperlipidaemia. by affecting the metabolic pathways of linoleic acid metabolism and alanine, aspartate and glutamate metabolism. Fatty liver is closely associated with changes in the biosynthesis pathway of pahenylalanine, tyrosine, and tryptophan in HUA patients with hyperlipidaemia. Changes in the glycine, serine and threonine metabolism pathway in HUA patients with hyperlipidaemia may lead to chronic kidney disease.
摘要：
背景：高尿酸血症和高脂血症都是彼此密切相关的常见代谢性疾病，两者都是各种疾病发展的独立危险因素。HUA合并高脂血症会增加非酒精性脂肪性肝病和冠心病的风险。本研究旨在探讨HUA与高脂血症的关系，并利用代谢组学研究HUA合并高脂血症患者的代谢途径变化。
方法：这是一项病例对照研究。调查2018年天津市协和医学中心体检人群HUA患者高脂血症患病率。使用Orbitrap质谱对308例HUA患者和100例正常对照进行代谢组学分析。30例无症状HUA患者的进一步代谢组学研究，30例高脂血症HUA患者，并进行了30名年龄和性别匹配的健康对照。通过正交偏最小二乘判别分析从三组中获得差异代谢物,并使用MetaboAnalyst5.0软件分析相关代谢途径的变化。
结果：HUA患者高脂血症患病率为69.3%。代谢组学分析发现,与对照组相比,33种不同的代谢物，包括花生四烯酸,丙氨酸,天冬氨酸,苯丙氨酸和酪氨酸，在无症状的HUA患者中发现。路径分析显示,这些变化主要与3个代谢通路有关,包括丙氨酸,天冬氨酸和谷氨酸代谢途径。38种不同的代谢物，包括亚油酸,丝氨酸,谷氨酸,和酪氨酸，在HUA高脂血症患者中发现。通路分析表明,它们主要与7条代谢通路有关,包括亚油酸代谢途径,苯丙氨酸,酪氨酸和色氨酸生物合成途径，和甘氨酸,丝氨酸和苏氨酸代谢途径。
结论：与普通人群相比，HUA人群的高脂血症发生率较高.HUA可引起高脂血症。通过影响亚油酸代谢和丙氨酸的代谢途径，天冬氨酸和谷氨酸代谢。脂肪肝与苯丙氨酸生物合成途径的变化密切相关,酪氨酸,和色氨酸在HUA高脂血症患者中的应用。甘氨酸的变化，HUA高脂血症患者的丝氨酸和苏氨酸代谢通路可能导致慢性肾脏病。
方法：这是一项病例对照研究。调查2018年天津市协和医学中心体检人群HUA患者高脂血症患病率。使用Orbitrap质谱对308例HUA患者和100例正常对照进行代谢组学分析。30例无症状HUA患者的进一步代谢组学研究，30例高脂血症HUA患者，并进行了30名年龄和性别匹配的健康对照。通过正交偏最小二乘判别分析从三组中获得差异代谢物,并使用MetaboAnalyst5.0软件分析相关代谢途径的变化。
结果：HUA患者高脂血症患病率为69.3%。代谢组学分析发现,与对照组相比,33种不同的代谢物，包括花生四烯酸,丙氨酸,天冬氨酸,苯丙氨酸和酪氨酸，在无症状的HUA患者中发现。路径分析显示,这些变化主要与3个代谢通路有关,包括丙氨酸,天冬氨酸和谷氨酸代谢途径。38种不同的代谢物，包括亚油酸,丝氨酸,谷氨酸,和酪氨酸，在HUA高脂血症患者中发现。通路分析表明,它们主要与7条代谢通路有关,包括亚油酸代谢途径,苯丙氨酸,酪氨酸和色氨酸生物合成途径，和甘氨酸,丝氨酸和苏氨酸代谢途径。
结论：与普通人群相比，HUA人群的高脂血症发生率较高.HUA可引起高脂血症。通过影响亚油酸代谢和丙氨酸的代谢途径，天冬氨酸和谷氨酸代谢。脂肪肝与苯丙氨酸生物合成途径的变化密切相关,酪氨酸,和色氨酸在HUA高脂血症患者中的应用。甘氨酸的变化，HUA高脂血症患者的丝氨酸和苏氨酸代谢通路可能导致慢性肾脏病。
