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This Article Full Text Full Text (PDF) All Versions of this Article: 287/6/G1168    most recent 00219.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (18) Citing Articles via Google Scholar Google Scholar Articles by Gaudier, E. Articles by Hoebler, C. Search for Related Content PubMed PubMed Citation Articles by Gaudier, E. Articles by Hoebler, C.

MUCOSAL BIOLOGY

Butyrate specifically modulates MUC gene expression in intestinal epithelial goblet cells deprived of glucose

¹Human Nutrition and Gut Function Department, Institut National de la Recherche Agronomique (INRA), 44316 Nantes; ²Institut National de la Santé et de la Recherche Médicale (INSERM) U539, 44035 Nantes; ³INSERM U560, 59045 Lille; and ⁴Food Safety and Nutrition Department, INRA, 78352 Jouy en Josas, France

Submitted 14 May 2004 ; accepted in final form 4 August 2004

The mucus layer covering the gastrointestinal mucosa is considered the first line of defense against aggressions arising from the luminal content. It is mainly composed of high molecular weight glycoproteins called mucins. Butyrate, a short-chain fatty acid produced during carbohydrate fermentation, has been shown to increase mucin secretion. The aim of this study was to test 1) whether butyrate regulates the expression of various MUC genes, which are coding for protein backbones of mucins, and 2) whether this effect depends on butyrate status as the major energy source of colonocytes. Butyrate was provided at the apical side of human polarized colonic goblet cell line HT29-Cl.16E in glucose-rich or glucose-deprived medium. In glucose-rich medium, butyrate significantly increased MUC3 and MUC5B expression (1.6-fold basal level for both genes), tended to decrease MUC5AC expression, and had no effect on MUC2 expression. In glucose-deprived medium, i.e., when butyrate was the only energy source available, MUC3 and MUC5B increase persisted, whereas MUC5AC expression was significantly enhanced (3.7-fold basal level) and MUC2 expression was strikingly increased (23-fold basal level). Together, our findings show that butyrate is able to upregulate colonic mucins at the transcriptional level and even better when it is the major energy source of the cells. Thus the metabolism of butyrate in colonocytes is closely linked to some of its gene-regulating effects. The distinct effects of butyrate according to the different MUC genes could influence the composition and properties of the mucus gel and thus its protective function.

mucin; short-chain fatty acids; energy source; human colonic cell line

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