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Am J Physiol Gastrointest Liver Physiol 284: G583-G587, 2003. First published December 4, 2002; doi:10.1152/ajpgi.00482.2002
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Vol. 284, Issue 4, G583-G587, April 2003

Intestinal alkaline phosphatase release is not associated with chylomicron formation

Andromeda M. Nauli, Shuqin Zheng, Qing Yang, Ronggui Li, Ronald Jandacek, and Patrick Tso

Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0529

Intestinal alkaline phosphatase (IAP) is one of the major sources of alkaline phosphatase in circulation. It is secreted into the intestinal lumen, serum, and lymph. After the ingestion of lipid, lymphatic alkaline phosphatase secretion increases significantly. We have found that the nonabsorbable 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 reesterification to form triacylglycerols, but not the formation of chylomicrons, that is necessary for the stimulation of the secretion of alkaline phosphatase into the lymph.

lymphatic alkaline phosphatase; Pluronic L-81; lipid; olestra


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Disruption of the murine intestinal alkaline phosphatase gene Akp3 impairs lipid transcytosis and induces visceral fat accumulation and hepatic steatosis
Am J Physiol Gastrointest Liver Physiol, May 1, 2007; 292(5): G1439 - G1449.
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