![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Wolfson Centre for Age-Related Disease, GKT School of Biomedical Science, King’s College London, London, SE1 9RT, UK
3To whom correspondence should be addressed. E-mail: jeremy.spencer{at}kcl.ac.uk.
There is considerable interest in the bioavailability of flavan-3-ols such as tea catechins and their bioactivity in vivo. Although flavanols such as catechin and epicatechin have long been characterized as powerful antioxidants in vitro, evidence suggests that these compounds undergo significant metabolism and conjugation during absorption in the small intestine and in the colon. In the small intestine these modifications lead primarily to the formation of glucuronide conjugates that are more polar than the parent flavanol and are marked for renal excretion. Other phase II processes lead to the production of O-methylated forms that have reduced antioxidant potential via the methylation of the B-ring catechol. Significant modification of flavanols also occurs in the colon where the resident microflora degrade them to smaller phenolic acids, some of which may be absorbed. Cell, animal and human studies have confirmed such metabolism by the detection of flavanol metabolites in the circulation and tissues. This review will highlight the major sites of flavanol metabolism in the gastrointestinal tract and the processes that give rise to potential bioactive forms of flavan-3-ols in vivo.
KEY WORDS: • flavonoid • metabolism • catechin • tea • GI tract
This article has been cited by other articles:
|
|
 |
|
  A. Y. Issa, S. R. Volate, S. J. Muga, D. Nitcheva, T. Smith, and M. J. Wargovich Green tea selectively targets initial stages of intestinal carcinogenesis in the AOM-ApcMin mouse model Carcinogenesis, September 1, 2007; 28(9): 1978 - 1984. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Lin, S. M. Zhang, K. Wu, W. C. Willett, C. S. Fuchs, and E. Giovannucci Flavonoid Intake and Colorectal Cancer Risk in Men and Women Am. J. Epidemiol., October 1, 2006; 164(7): 644 - 651. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Rein, E. Schijlen, T. Kooistra, K. Herbers, L. Verschuren, R. Hall, U. Sonnewald, A. Bovy, and R. Kleemann Transgenic Flavonoid Tomato Intake Reduces C-Reactive Protein in Human C-Reactive Protein Transgenic Mice More Than Wild-Type Tomato J. Nutr., September 1, 2006; 136(9): 2331 - 2337. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Chen, L. Cui, X. Duan, B. Ma, and D. Zhong PHARMACOKINETICS AND METABOLISM OF THE FLAVONOID SCUTELLARIN IN HUMANS AFTER A SINGLE ORAL ADMINISTRATION Drug Metab. Dispos., August 1, 2006; 34(8): 1345 - 1352. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Possemiers, S. Bolca, C. Grootaert, A. Heyerick, K. Decroos, W. Dhooge, D. De Keukeleire, S. Rabot, W. Verstraete, and T. Van de Wiele The Prenylflavonoid Isoxanthohumol from Hops (Humulus lupulus L.) Is Activated into the Potent Phytoestrogen 8-Prenylnaringenin In Vitro and in the Human Intestine J. Nutr., July 1, 2006; 136(7): 1862 - 1867. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Vanamala, T. Leonardi, B. S. Patil, S. S. Taddeo, M. E. Murphy, L. M. Pike, R. S. Chapkin, J. R. Lupton, and N. D. Turner Suppression of colon carcinogenesis by bioactive compounds in grapefruit Carcinogenesis, June 1, 2006; 27(6): 1257 - 1265. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. L Keen, R. R Holt, P. I Oteiza, C. G Fraga, and H. H Schmitz Cocoa antioxidants and cardiovascular health Am. J. Clinical Nutrition, January 1, 2005; 81(1): 298S - 303S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. M. Mutch, R. Simmering, D. Donnicola, G. Fotopoulos, J. A. Holzwarth, G. Williamson, and I. Corthesy-Theulaz Impact of commensal microbiota on murine gastrointestinal tract gene ontologies Physiol Genomics, September 16, 2004; 19(1): 22 - 31. [Abstract] [Full Text] [PDF]
|
|
