Journal
JOURNAL OF PROTEOME RESEARCH
Volume 9, Issue 5, Pages 2527-2538Publisher
AMER CHEMICAL SOC
DOI: 10.1021/pr901203w
Keywords
dietary cholesterol; H-1 NMR spectroscopy; liver steatosis; LDLr-deficient mice; metabolomics quantitative profiling; NASH
Categories
Funding
- Fond de Investigacion Sanitaria (FIS) [PI051606, PI08/1381]
- CIBER de Diabetes y Enfermedades Metabolicas (CIBERDEM)
- Generalitat de Catalunya [FI-G 0503]
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Nonalcoholic fatty liver disease is considered to be the hepatic manifestation of metabolic syndrome and is usually related to high-fat, high-cholesterol diets. With the rationale that the identification and quantification of metabolites in different metabolic pathways may facilitate the discovery of clinically accessible biomarkers, we report the use of H-1 NMR metabolomics for quantitative profiling of liver extracts from LDLr-/- mice, a well-documented mouse model of fatty liver disease. A total of 55 metabolites were identified, and multivariate analyses in a diet- and time-comparative strategy were performed. Dietary cholesterol increased the hepatic concentrations of cholesterol, triglycerides, and oleic acid but also decreased the [PUFA/MUFA] ratio as well as the relative amount of long-chain polyunsaturated fatty acids in the liver. This was also accompanied by variations of the hepatic concentration of taurine, glutathione, methionine, and carnitine. Heat-map correlation analyses demonstrated that hepatic inflammation and development of steatosis correlated with cholesterol and triglyceride NMR derived signals, respectively. We conclude that dietary cholesterol is a causal factor in the development of both liver steatosis and hepatic inflammation.
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