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Journal of Nutrition Vol. 110 No. 1 January 1980, pp. 178-188
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The Prevalence, Metabolism and Migration of Goblet Cells in Rat Intestine following the Induction of Rapid, Synchronous Vitamin A Deficiency1,2,

Wannee Rojanapo3, Adrian J. Lamb4 and James A. Olson5

Department of Biochemistry, Faculty of Science, Mahidol University, Rama VI Road, Bangkok 4, Thailand

Experiments were conducted to evaluate critically the role of vitamin A in the maintenance and functional integrity of mucus-secreting goblet cells in rat small intestine. Essentially synchronous vitamin A deficiency was induced by the withdrawal of retinoic acid from mature, stringently-deficient male rats reared by feeding vitamin A-depleted weanlings diets first supplemented with and then lacking in 2 µg retinoic acid per gram diet in repeating 18 day:10 day cycles. Secondary inanition was minimized by force-feeding both deficient and control animals twice daily. Whereas the prevalence of oligomucus cells was unchanged, the number of goblet cells per duodenal crypt gland decreased abruptly to 60% of control values starting 2 to 3 days after the withdrawal of retinoic acid and then stabilized. The responses of mucus-secreting cells to atropine and pilocarpine were identical in vitamin A deficient and control animals. As studied with [3H]thymidine, the rate of division of epithelial cells and the migration rate of columnar and goblet cells out of the crypt gland and along the villus were also unaffected by vitamin A deficiency. We conclude that two populations of goblet cells exist in the intestine—one relatively insensitive and the other sensitive to vitamin A status. In vitamin A deficiency, the rate of differentiation of sensitive goblet cells from oligomucus cells and other precursor cells seems to be blocked.


KEY WORDS: • retinoic acid • synchronous vitamin A deficiency • rat intestinal goblet cells • intestinal cell migration rates

1 Supported in part by U.S. National Institutes of Health Grant No. NIH-AM-11367 and the Faculty of Graduate Studies, Mahidol University.

2 Taken in part from a thesis submitted by Ms. Wannee Rojanapo to the Faculty of Graduate Studies, Mahidol University in partial fulfillment of the requirement for a Ph.D. degree.

3 Present address: Research Division, National Cancer Institute, Ministry of Public Health, Rama VI Rd., Bangkok 4, Thailand.

4 To whom reprint requests should be sent.

5 Present address: Department of Biochemistry and Biophysics, Iowa State University, Ames, IA 50011, U.S.A.

Manuscript received 29 May 1979.





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