Serum metabonomics of NAFLD plus T2DM based on liquid chromatography–mass spectrometry

Chen, Yang; Li, Chunlong; Liu, Liyan; Guo, Fuchuan; Li, Songtao; Huang, Lina; Sun, Chongde; Feng, Rennan

doi:10.1016/j.clinbiochem.2016.05.016

Cited by 24 publications

(13 citation statements)

References 13 publications

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“…These pathways include: a, aminoacyl-tRNA biosynthesis; b, primary bile acid biosynthesis; c, citrate cycle TCA cycle); d, alanine; aspartate and glutamate metabolism; e, methane metabolism; f, propanoate metabolism; g, D-Glutamine and D-glutamate metabolism; h, nitrogen metabolism; i, butanoate metabolism; j, glyoxylate and dicarboxylate metabolism; k, cyanoamino acid metabolism. with our results, increased serum level of proline has been shown in subjects with NAFLD (30). Also previous studies showed that patients with alcoholic and non-alcoholic liver diseases had high mRNA expression of procollagen compared to the controls (31).…”

Section: Amino Acid Metabolismsupporting

confidence: 89%

Metabolomic Biomarkers in the Diagnosis of Non-Alcoholic Fatty Liver Disease

et al. 2019

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Background: Nonalcoholic fatty liver disease (NAFLD) is the most abundant chronic liver disorder, because racial and ethnic differences may influence prevalence and severity of NAFLD. Objectives: This metabolomic study was conducted to identify the metabolic biomarkers and determine the mechanism of progress of NAFLD in Iranian patients. Methods: Serum samples were collected from 75 participants (37 healthy controls and 38 patients with NAFLD) after an overnight fast. The metabolome of all samples were determined by nuclear magnetic resonance (NMR) and were compared by multivariate statistical analysis. Results: Totally, 19 metabolomic biomarkers were identified by NMR. Compared to healthy controls, NAFLD patients had increased serum concentrations of glycochenodeoxycholic acid, taurocholic acid, glycocholic acid, deoxycholic acid, valine, isoleucine, succinic acid, isocitric acid, 2-ketoglutaric acid, trimethylamine, proline, hydroxyproline and tyrosine, while the concentrations of butyric acid, propionic acid, isovaleric acid, glutamine, glycine, and serine decreased. Conclusions: A robust set of biomarkers for diagnosis of NAFLD was established. Serum metabolomics biomarkers revealed changes in some amino acids and their derivatives, bile acids, short chain fatty acids, and tricarboxylic acid cycle intermediates in subjects with NAFLD compared to healthy controls. These markers could be used as indicators regarding the efficacy of therapeutic interventions.

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Section: Amino Acid Metabolismsupporting

confidence: 89%

Metabolomic Biomarkers in the Diagnosis of Non-Alcoholic Fatty Liver Disease

et al. 2019

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“…A metabolomic study of Chinese NAFLD patients with and without type-2 diabetes mellitus (T2DM) reported elevated bilirubin, various amino acids, and acyl carnitines, together with oleamide [206]. Many of these metabolic changes were confirmatory of published studies.…”

Section: Nafl and Nashmentioning

confidence: 67%

Metabolomic and Lipidomic Biomarkers for Premalignant Liver Disease Diagnosis and Therapy

Beyoğlu

Idle

2020

Metabolites

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In recent years, there has been a plethora of attempts to discover biomarkers that are more reliable than α-fetoprotein for the early prediction and prognosis of hepatocellular carcinoma (HCC). Efforts have involved such fields as genomics, transcriptomics, epigenetics, microRNA, exosomes, proteomics, glycoproteomics, and metabolomics. HCC arises against a background of inflammation, steatosis, and cirrhosis, due mainly to hepatic insults caused by alcohol abuse, hepatitis B and C virus infection, adiposity, and diabetes. Metabolomics offers an opportunity, without recourse to liver biopsy, to discover biomarkers for premalignant liver disease, thereby alerting the potential of impending HCC. We have reviewed metabolomic studies in alcoholic liver disease (ALD), cholestasis, fibrosis, cirrhosis, nonalcoholic fatty liver (NAFL), and nonalcoholic steatohepatitis (NASH). Specificity was our major criterion in proposing clinical evaluation of indole-3-lactic acid, phenyllactic acid, N-lauroylglycine, decatrienoate, N-acetyltaurine for ALD, urinary sulfated bile acids for cholestasis, cervonoyl ethanolamide for fibrosis, 16α-hydroxyestrone for cirrhosis, and the pattern of acyl carnitines for NAFL and NASH. These examples derive from a large body of published metabolomic observations in various liver diseases in adults, adolescents, and children, together with animal models. Many other options have been tabulated. Metabolomic biomarkers for premalignant liver disease may help reduce the incidence of HCC.

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“…The energy metabolism impairment was also partly proved by the accumulation of gluconic acid, which might be resulted from the inhibitation of glucose metabolism. Meanwhile, it was also reported that palmitoylcarnitine and linoleyl carnitine were significantly increased in patients with liver disease such as nonalcoholic fatty liver disease (NAFLD) and chronic liver failure [ 24 , 25 ]. HFD could destroy the equilibrium between the formation and degradation of lipid, and lead to excessive lipid deposition in hepatocytes, resulting disorder of liver function.…”

Section: Discussionmentioning

confidence: 99%

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

Liu

Kong

et al. 2017

Lipids Health Dis

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BackgroundBased on the pro-drug principle, aspirin and eugenol were esterified to synthesize aspirin eugenol ester (AEE). The anti-hyperlipidemia effect of aspirin eugenol ester has been confirmed in hyperlipidemic rat induced by high fat diet (HFD). However, its effect on liver and feces metabonomic profiles remains unknown.MethodsSuspension of AEE was prepared in 5% carboxymethyl cellulose sodium (CMC-Na). Thirty rats were divided into control, model and AEE groups. The control and model rats were fed with normal diet or HFD for 13 weeks, respectively. Rats in AEE-treated group were fed with HFD for 8 weeks to induce hyperlipidemia, and then given AEE once daily by oral gavage for 5 weeks at the dosage of 54 mg/kg body weight. After drug intervention, lipid profile analysis and oil red O staining were carried out to confirm the lipid accumulation in liver tissue. UPLC-Q-TOF/MS-based liver and feces metabonomics coupled with pathway analysis were conducted to evaluate the changes of metabolic profile and endogenous metabolites.ResultsIn liver tissue, oral administration of AEE significantly reduced lipid droplets and the levels of triglyceride (TG) and low-density lipoprotein (LDL). Using principal component analysis (PCA) and partial least squares-discriminate analysis (PLS-DA), distinct changes in metabolite patterns in feces and liver were observed. Liver and feces samples in control, model and AEE groups were scattered in PLS-DA score plots. 28 metabolites in liver and 22 in feces were identified as potential biomarkers related to hyperlipidemia. As possible drug targets, the perturbations of those biomarkers can be regulated by administration of AEE.ConclusionAnti-hyperlipidemia effect of AEE was confirmed by lipid analysis, oil red O staining and metabolomics analysis. The mechanism of AEE might be associated with the changes in the metabolism of glycerophospholipid, amino acid, fatty acid, sphingolipid, purine, bile acid and glutathione.Electronic supplementary materialThe online version of this article (10.1186/s12944-017-0633-0) contains supplementary material, which is available to authorized users.

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Serum metabonomics of NAFLD plus T2DM based on liquid chromatography–mass spectrometry

Cited by 24 publications

References 13 publications

Metabolomic Biomarkers in the Diagnosis of Non-Alcoholic Fatty Liver Disease

Metabolomic Biomarkers in the Diagnosis of Non-Alcoholic Fatty Liver Disease

Metabolomic and Lipidomic Biomarkers for Premalignant Liver Disease Diagnosis and Therapy

Feces and liver tissue metabonomics studies on the regulatory effect of aspirin eugenol eater in hyperlipidemic rats

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