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Articles in PresS, published online ahead of print December 4, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00482.2002
Submitted on November 7, 2002
Accepted on December 1, 2002
1 Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: tsopp{at}email.uc.edu.
Intestinal alkaline phosphatase is one of the major sources of alkaline phosphatase in circulation. It is secreted into the intestinal lumen, serum, and lymph. Following the ingestion of lipid, lymphatic alkaline phosphatase secretion increases significantly. We have found that the non-absorbable fat, olestra, is unable to stimulate lymphatic alkaline phosphatase secretion. We also found that the hydrophobic surfactant, Pluronic L-81, which blocks chylomicron formation, fails to inhibit this increase in lymphatic alkaline phosphatase secretion. These results suggest that it is the lipid uptake into the mucosa and/or re-esterification to form triacylglycerols, but not the formation of chylomicrons, that is necessary for the stimulation of the secretion of alkaline phosphatase into the lymph.
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