Re: IBD & Dioxins Link?

TCDD-induced change in intestinal function and pathology: evidence for
the involvement of arylhydrocarbon receptor-mediated alteration of
glucose trans****tation.

Although numerous studies have been performed to clarify the
mechanism(s) underlying the toxicological responses induced by
dioxins, their effect on the intestine is less well understood. To
address this issue, we examined the effect of TCDD on the pathology
and function of the intestine in arylhydrocarbon receptor (AhR)-
sensitive (C57BL/6J) and -less-sensitive (DBA/2J) mice. A single oral
administration of TCDD (100 mug/kg) to C57BL/6J mice produced changes
in villous structure and nuclear/cytoplasm ratio in the epithelial
cells of the intestine. Furthermore, in an oral glucose tolerance
test, the serum glucose level was significantly increased in the C57BL/
6J mouse but not in the DBA/2J mouse by TCDD treatment. In agreement
with this, the expression of intestinal mRNAs coding sodium-glucose co-
trans****ter 1 (SGLT1) and glucose trans****ter type 2 were increased
only in C57BL/6J mice by TCDD. The increase in the former trans****ter
was also confirmed from its protein level. The glucose level in the
intestinal contents is thought to be one of the factors contributing
to SGLT1 induction. Concerning with this, the intestinal activity of
sucrase and lactase was significantly increased only in C57BL/6J mice
by TCDD. These results suggest that while TCDD produces initial damage
to the intestinal epithelium, the tissues induce SGLT1 to facilitate
the absorption of glucose, which is expected, at least partially, to
combat the wasting syndrome induced by TCDD. The data provided here
also suggest that AhR is involved in the mechanism of SGLT1 induction.
PMID: 15885268