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Overcoming developmental limitations to intestinal sugar transport: the role of glucocorticoids.
Author(s) -
douard veronique,
Choi HoyIn,
Ferraris Ronaldo P
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1322-d
Subject(s) - endocrinology , medicine , glucocorticoid receptor , glucocorticoid , mineralocorticoid , receptor , dexamethasone , chemistry , fructose , d glucose , biology , biochemistry
Under normal conditions, rat intestinal GLUT5 expression and activity can be induced only by its substrate fructose (F) and only after 14 d of age. We showed that > 4 h after dexamethasone (D, a glucocorticoid analog) administration, F perfusion stimulated GLUT5 in 10 d old pups, suggesting that D allows F to precociously induce its transporter. D binds the glucocorticoid (GR), mineralocorticoid (MR) and pregnane‐X (PXR) receptors we determined to be significantly expressed in 10 d old intestines. To identify the receptor/s involved in the D‐mediated, F‐induced precocious development of GLUT5, 10 d old pups were injected with vehicle alone, D alone, and D with various doses of RU486 (RU) or spironolactone (S) (GR or MR antagonists, respectively). RU prevented the D‐mediated effects on body weight, arginase (gene known to be regulated by GR) and F‐induced GLUT5 expression and activity. In contrast, S did not block any of the effects of D. RU and S are also agonists of PXR. Injection of various doses of RU or S alone did not affect body weight and GLUT5, indicating that PXR is not involved in their regulation. D, D+RU, D+S, RU and S each had no effect on SGLT1 expression and activity, suggesting that the effects of D and RU on GLUT5 are specific. The precocious development of GLUT5 in F‐perfused intestines of 10 d old pups induced by D appears to be mediated solely and specifically by the GR. (NSF‐IBN235011)