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Metabolic pathway analysis of hyperuricaemia patients with hyperlipidaemia based on high-throughput mass
Xue Wei1, Xiaodong Jia1, Rui Liu2
1Tianjin Union Medical Center, Tianjin Medical University, Tianjin, 300070, China.
Insights
Hyperuricaemia (HUA) significantly increases hyperlipidaemia risk, impacting metabolic pathways like linoleic acid and amino acid metabolism. These changes are linked to fatty liver and kidney disease development in affected individuals.
Area of Science:
- Metabolomics
- Biochemistry
- Internal Medicine
Background:
- Hyperuricaemia (HUA) and hyperlipidaemia are common metabolic diseases independently linked to various health risks.
- Their co-occurrence exacerbates the risk of nonalcoholic fatty liver disease and coronary heart disease.
- Understanding the metabolic interplay between HUA and hyperlipidaemia is crucial for disease management.
Purpose of the Study:
- To investigate the relationship between hyperuricaemia (HUA) and hyperlipidaemia.
- To identify metabolic pathway alterations in patients with co-existing HUA and hyperlipidaemia using metabolomics.
Main Methods:
- A case-control study analyzed 308 HUA patients and 100 controls using Orbitrap mass spectrometry.
- A subset of 30 asymptomatic HUA patients, 30 HUA patients with hyperlipidaemia, and 30 healthy controls underwent detailed metabolomics analysis.
- Orthogonal partial least-squares discriminant analysis identified differential metabolites, with pathway analysis performed using MetaboAnalyst 5.0.
Main Results:
- The prevalence of hyperlipidaemia in HUA patients was 69.3%.
- Asymptomatic HUA patients showed 33 differential metabolites linked to alanine, aspartate, and glutamate metabolism.
- HUA patients with hyperlipidaemia exhibited 38 differential metabolites associated with linoleic acid metabolism, phenylalanine/tyrosine/tryptophan biosynthesis, and glycine/serine/threonine metabolism.
Conclusions:
- HUA significantly increases hyperlipidaemia incidence by altering linoleic acid and alanine, aspartate, and glutamate metabolism pathways.
- Fatty liver risk in HUA patients with hyperlipidaemia correlates with altered phenylalanine, tyrosine, and tryptophan biosynthesis.
- Changes in glycine, serine, and threonine metabolism may indicate a risk for chronic kidney disease in HUA patients with hyperlipidaemia.
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.
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