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Volume 18, Issue 3, Pages 163-167 (March 2007)


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Enterohepatic circulation of organochlorine compounds: a site for nutritional intervention

Ronald J. JandacekCorresponding Author Informationemail address, Patrick Tso

Received 10 January 2006; accepted 13 December 2006.

Refers to erratum:
Erratum to “Enterohepatic circulation of organochlorine compounds: a site for nutritional intervention” [J Nutr Biochem 18 (2007) 163–167]
Ronald J. Jandacek, Patrick Tso
The Journal of Nutritional Biochemistry
May 2007 (Vol. 18, Issue 5, Page 355)
Full Text | Full-Text PDF (64 KB)

Abstract 

Organochlorine compounds enter the body primarily as components of the diet. Their removal from the body is via excretion into the feces. There is evidence that many people are in a positive balance, with the rate of intake of organochlorines exceeding that of their excretion. A desirable nutritional approach to this problem would both reduce dietary intake and increase fecal excretion. Nonabsorbable dietary lipids reduce the absorption of dietary organochlorines and also increase the rate of their fecal excretion. Organochlorine compounds that are stored in the body enter the intestine both in bile and through a poorly understood nonbiliary mechanism. Part of the amount that enters the intestine is excreted, and part is reabsorbed in an enterohepatic circulation. There is evidence that an increase in excretion can be achieved by interference with the enterohepatic circulation of organochlorine compounds and their metabolites. Data from animals and humans show that the presence of nonabsorbed lipid in the intestine can increase the rate of excretion in a clinically significant manner.

Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, OH 45237, USA

Corresponding Author InformationCorresponding author.Tel.: +1 15135585492; fax: +1 5135581312.

 This study was funded by The National Research Initiative of the USDA Cooperative State Research Education and Extension Service, Grant number 02-00824, and by Glaxo SmithKline.

PII: S0955-2863(06)00269-5

doi:10.1016/j.jnutbio.2006.12.001


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