MITOME Hidemichi    Department   Matsuyama University  School of Clinical Pharmacy, College of Pharmaceutical Sciences    Position   Associate professor
Language	English
Publication Date	2013/07
Type
Peer Review	With peer review
Title	Metabonomic study on the biochemical response of spontaneously hypertensive rats to chronic taurine supplementation using 1H NMR spectroscopic urinalysis
Contribution Type
Journal	Journal of Pharmaceutical and Biomedical Analysis
Volume, Issue, Pages	85,pp.155-161
Author and coauthor	Kazuki Akira, Hiroyuki Hichiya, Mayu Morita, Akane Shimizu, Hidemichi Mitome
Details	There is a wealth of exptl. information and some clin. evidence available in the literature suggesting that taurine exerts preventive effects on cardiovascular diseases. In particular, taurine has been shown to reduce blood pressure in not only hypertensive patients but also in a no. of hypertensive rodent models such as spontaneously hypertensive rats (SHR). However, the mol. basis of the efficacy and toxicity of the compd. has not been fully characterized. We have investigated the effects of taurine supplementation to urinary low-mol.-wt. endogenous metabolites in SHR using a 1H NMR-based urinary metabolomic approach. The SHR were chronically treated with 3\% taurine in drinking water from four to 14 wk of age, and 24-h urine samples were analyzed using 1H NMR spectroscopy. Metabolic information was extd. from the NMR data by principal components anal. as well as visual inspection. Consequently, the metabolite profile started to change with considerable interindividual variation from six weeks of age. The extent of change became increasingly remarkable with the duration of treatment, with the concurrent observation of the hypotensive effect. The metabolic changes included a decreased urinary output of tricarboxylic acid cycle intermediates (citrate, α-ketoglutarate, and succinate) and an increased output of phenylacetylglycine and p-cresol sulfate. The results suggest that chronic taurine supplementation to the SHR resulted in an acceleration of metabolic acidosis with perturbation in the tricarboxylic acid cycle and the modulation of the intestinal microbial metab.