Taurine synthesis in isolated rat hepatocytes in suspension exposed to carbon tetrachloride

Waterfield, CJ; Ja, Turton; Scales,; Timbrell, JA

doi:10.1042/bst0181218

Cited by 7 publications

(3 citation statements)

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“…Therefore, the author speculated that the increasing taurine excretion was associated with an older subject age. Increased urinary taurine has been suggested to be a marker of liver damage. , In our study, taurine was significantly positively correlated with liver weight. Since the liver is the most metabolically active organ in the body, it would not be surprising that the altered metabolism in obese WKY and SHR negatively affected this organ and its metabolic functions.…”

Section: Resultssupporting

confidence: 65%

Metabolomic Study of Obesity and Its Treatment with Palmitoylated Prolactin-Releasing Peptide Analog in Spontaneously Hypertensive and Normotensive Rats

et al. 2019

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In this study, the combination of metabolomics and standard biochemical and biometric parameters was used to describe the metabolic effects of diet-induced obesity and its treatment with the novel antiobesity compound palm 11 -PrRP31 (palmitoylated prolactin-releasing peptide) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). The results showed that SHR on a high-fat (HF) diet were normoglycemic with obesity and hypertension, while WKY on the HF diet were normotensive and obese with prediabetes. NMR-based metabolomics revealed mainly several microbial cometabolites altered by the HF diet, particularly in urine. The HF diet induced similar changes in both models. However, two groups of genotype-specific metabolites were defined: metabolites specific to the genotype at baseline (e.g., 1-methylnicotinamide, phenylacetylglycine, taurine, methylamine) and metabolites reacting specifically to the HF diet in individual genotypes (2-oxoglutarate, dimethylamine, N-butyrylglycine, p-cresyl sulfate). The palm 11 -PrRP31 lowered body weight and improved biochemical and biometric parameters in both strains, and it improved glucose tolerance in WKY rats on the HF diet. In urine, the therapy induced significant decrease of formate and 1-methylnicotinamide in SHR and alanine, allantoin, dimethylamine, and Nbutyrylglycine in WKY. Altogether, our study confirms the effectiveness of palm 11 -PrRP31 for antiobesity treatment.

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Section: Resultssupporting

confidence: 65%

Metabolomic Study of Obesity and Its Treatment with Palmitoylated Prolactin-Releasing Peptide Analog in Spontaneously Hypertensive and Normotensive Rats

et al. 2019

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“…The observed elevation of taurine in the urine of dosed mice was also concurrent with this notion, since taurine is an antioxidant and an organic osmolyte capable of protecting and stabilizing cells. 46 Furthermore, the observation of marked elevation of nucleotides, such as uridine and inosine in the liver extracts of mequindox exposed mice, provided an additional support for the association of liver damage with mequindox injury since higher nucleosides revealed the RNA degradation. Our observation is in good agreement with previously observed effects of long-term mequindox exposure on the liver.…”

Section: ' Discussionmentioning

confidence: 93%

Dynamic Metabolic Response of Mice to Acute Mequindox Exposure

et al. 2011

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Mequindox is used as a veterinary antibiotic drug. As part of systematic investigations into mequindox as a veterinary medicine and its subsequent applications in food safety, we conducted the investigation to assess the metabolic response of mice to mequindox using metabonomics, which combines NMR metabolic profiles of biofluids or tissues and pattern recognition data analysis. In this study, we delivered a single dose of mequindox to mice with dosage levels of 15, 75, and 350 mg/kg body weight and collected urine samples over a 7 day period, as well as plasma and liver tissues at 7 days postdose. Principal components analysis (PCA) and orthogonal projection to latent structure discriminant analysis (O-PLS-DA) were performed on (1)H NMR spectra of biofluids and liver, showing that low dose levels of mequindox exposure had no adverse effects, consistent with histological observations of the liver. High and moderate levels of mequindox exposure caused suppression of glycolysis and stimulation of fatty acid oxidation accompanied with increased levels of oxidative stress. Our metabonomic analyses also showed disruption of amino acid metabolism, consistent with liver damage observed from histopathological examinations. Furthermore, mequindox perturbed gut microbial activity manifested in the altered excretion of urinary trimethylamine (TMA), trimethylamine-N-oxide (TMAO), hippurate, phenylacetylglycine (PAG), and phenylacetate. The putative gut microbial function may also contribute to the assembly and secretion of very-low-density lipoproteins from the liver to the plasma. Our work provides important insights on the metabolic responses of mequindox.

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“…The treatment with liraglutide significantly decreased taurine levels compared with the untreated HF diet-fed group. Waterfield and coworkers suggested that increased urinary taurine could be a marker of liver damage (Waterfield et al 1990(Waterfield et al , 1991. Their results demonstrated that the liver damage, in their case induced by toxic insult, increased taurine synthesis and consequently taurine excretion into urine also.…”

Section: :1mentioning

confidence: 99%

The effects of liraglutide in mice with diet-induced obesity studied by metabolomics

Bugáňová

Pelantová

Holubová

et al. 2017

Journal of Endocrinology

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Liraglutide is the glucagon-like peptide-1 receptor agonist widely used for the treatment of type 2 diabetes mellitus. Recently, it has been demonstrated to decrease cardiovascular morbidity and mortality in patients with type 2 diabetes and high cardiovascular risk. Although the major modes of liraglutide action are well-known, its detailed action at the metabolic level has not been studied. To this end, we explored the effect of 2-week liraglutide treatment in C57BL/6 male mice with obesity and diabetes induced by 13 weeks of high-fat diet using NMR spectroscopy to capture the changes in urine metabolic profile induced by the therapy. The liraglutide treatment decreased body and fat pads weight along with blood glucose and triglyceride levels. NMR spectroscopy identified 11 metabolites significantly affected by liraglutide treatment as compared to high-fat diet-fed control group. These metabolites included ones involved in nicotinamide adenine dinucleotide metabolism, β-oxidation of fatty acids and microbiome changes. Although majority of the metabolites changed after liraglutide treatment were similar as the ones previously identified after vildagliptin administration in a similar mouse model, the changes in creatinine, taurine and trigonelline were specific for liraglutide administration. The significance of these changes and its possible use in the personalization of antidiabetic therapy in humans requires further research.

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Taurine synthesis in isolated rat hepatocytes in suspension exposed to carbon tetrachloride

Cited by 7 publications

References 0 publications

Metabolomic Study of Obesity and Its Treatment with Palmitoylated Prolactin-Releasing Peptide Analog in Spontaneously Hypertensive and Normotensive Rats

Metabolomic Study of Obesity and Its Treatment with Palmitoylated Prolactin-Releasing Peptide Analog in Spontaneously Hypertensive and Normotensive Rats

Dynamic Metabolic Response of Mice to Acute Mequindox Exposure

The effects of liraglutide in mice with diet-induced obesity studied by metabolomics

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