Posted on 01/27/2005 7:59:06 PM PST by Coleus
Am J Physiol Regul Integr Comp Physiol (November 24, 2004). doi:10.1152/ajpregu.00693.2004
1 Biological Science Laboratories, Kao Corporation, Haga-gun, Tochigi, Japan
* To whom correspondence should be addressed. E-mail: murase.takatoshi@kao.co.jp.
Green tea contains a high level of polyphenolic compounds known as catechins. We investigated the effects of green tea extract (GTE), which is rich in catechins on endurance capacity, energy metabolism and fat oxidation in Balb/c mice over a 10 week period. Swimming times to exhaustion for mice fed 0.2% - 0.5% (w/w) GTE were prolonged by 8% - 24% and the effects were dose dependent, and accompanied by lower respiratory quotients and higher rates of fat oxidation, as determined by indirect calorimetry. In addition, feeding with GTE increased the level of 
-oxidation activity in skeletal muscle. Plasma lactate concentrations in mice fed GTE were significantly decreased after exercise, concomitant with increases in free fatty acid concentrations in plasma, suggesting an increased lipid utilization as an energy source in GTE -fed mice. Epigallocatechin gallate (EGCG), a major component of tea catechins, also enhanced endurance capacity, suggesting that the endurance-improving effects of GTE were mediated, at least partly, by EGCG. The -oxidation activity and the level of fatty acid translocase (FAT/CD36) mRNA in the muscle was higher in GTE-fed mice compared to control mice. These results indicate that GTE are beneficial for improving endurance capacity and support the hypothesis that the stimulation of fatty acid utilization is a promising strategy for improving endurance capacity.
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INFLAMMATION/IMMUNITY/MEDIATORS
but not by IL-4Intestinal Disease Research Programme, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
Submitted 17 July 2003 ; accepted in final form 23 June 2004
A characteristic of many enteropathies is increased epithelial permeability, a potentially pathophysiological event that can be evoked by T helper (Th)-1 (i.e., IFN-
) and Th2 (i.e., IL-4) cytokines and bacterial infection [e.g., enteropathogenic Escherichia coli (EPEC)]. The green tea polyphenol (–)-epigallocatechin gallate (EGCG) has immunosuppressive properties, and we hypothesized that it would ameliorate the increased epithelial permeability induced by IFN-, IL-4, and/or EPEC. EGCG, but not the related epigallocatechin, completely prevented the increase in epithelial (i.e., T84 cell monolayer) permeability caused by IFN- exposure as gauged by transepithelial resistance and horseradish peroxidase flux; EGCG did not alleviate the barrier disruption induced by IL-4 or EPEC. IFN--treated T84 and THP-1 (monocytic cell line) cells displayed STAT1 activation (tyrosine phosphorylation on Western blot analysis, DNA binding on EMSA) and upregulation of interferon response factor-1 mRNA, a STAT1-dependent gene. All three events were inhibited by EGCG pretreatment. Aurintricarboxylic acid also blocked IFN--induced STAT1 activation, but it did not prevent the increase in epithelial permeability. Additionally, pharmacological blockade of MAPK signaling did not affect IFN--induced epithelial barrier dysfunction. Thus, as a potential adjunct anti-inflammatory agent, EGCG can block STAT1-dependent events in gut epithelia and monocytes and prevent IFN--induced increased epithelial permeability. The latter event is both a STAT1- and MAPK-independent event.
intestinal barrier; permeability; T84; signal transducer and activator of transcription-1
how much egcg is in it?
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