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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00428.2002
Submitted on July 17, 2002
Accepted on October 3, 2002
1 Medicine, Emory University School of Medicine, Atlanta, GA, USA
2 Medicine, Emory University School of Medicine, Atlanta, GA, USA; Nutrition and Health Sciences Program, Emory University School of Medicine, Atlanta, GA, USA
3 Pathology, Emory University School of Medicine, Atlanta, GA, USA
4 Medicine, Harvard Medical School, Boston, MA, USA
5 Pathology, Amgen Inc., Thousand Oaks, CA, USA
6 Biochemistry, Emory University School of Medicine, Atlanta, GA, USA; Nutrition and Health Sciences Program, Emory University School of Medicine, Atlanta, GA, USA
* To whom correspondence should be addressed. E-mail: tzieg01{at}emory.edu.
The trefoil factor family peptides TFF1, TFF2 and TFF3 are important for mucosal protection and restitution. KGF stimulates proliferation and differentiation of epithelial cells with potent effects on goblet cells. To investigate interactions between food intake and KGF, rats were fed ad libitum (control), fasted for 72 h or fasted for 72 h and then re-fed for 72 h, ±KGF (3 mg/kg/day). With fasting, goblet cell number in duodenum increased, TFF3 mRNA in duodenum and jejunum decreased and TFF3 protein did not change or increased. KGF during fasting stimulated colonic growth, normalized TFF3 mRNA in duodenum and jejunum and broadly up-regulated gut goblet cell number and TFF3 protein expression. With fasting/re-feeding, KGF increased small bowel and colonic mucosal growth, goblet cell number and TFF3 protein, but had variable effects on TFF3 mRNA. KGF specifically induced TFF2 mRNA and protein in the duodenum and jejunum with both nutritional regimens. We conclude that nutrient availability modifies rat intestinal goblet cell number, TFF3 mRNA and the gut-trophic effects of KGF in a region-specific manner. KGF enhances TFF2 expression in proximal small bowel and increases goblet cell number and TFF3 protein content throughout the intestine independent of food intake.
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