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Departments of Internal Medicine and Physiology, Division of Digestive Diseases, The Ohio State University School of Medicine, Columbus, Ohio 43210
Short-chain fatty acids (SCFA) have been demonstrated to
at least partially ameliorate chronic intestinal inflammation. However, whether and how intestinal SCFA absorption may be altered during chronic intestinal inflammation is unknown. A rabbit model of chronic
ileitis produced by coccidia was used to determine the effect of
chronic inflammation on ileal
SCFA/HCO
3 exchange.
SCFA/HCO
3 exchange was present in the
brush-border membrane (BBM) of villus but not crypt cells from normal
rabbit ileum. An anion-exchange inhibitor, DIDS, significantly inhibited SCFA/HCO
3 exchange.
Extravesicular Cl
did not alter the uptake of SCFA,
suggesting that SCFA/HCO
3 exchange is
a transport process distinct from
Cl
/HCO
3 exchange.
In chronically inflamed ileum, SCFA/HCO
3 exchange was also present
only in BBM of villus cells. The exchanger was sensitive to DIDS and
was unaffected by extravesicular Cl
. However,
SCFA/HCO
3 exchange was significantly reduced in villus cell BBM vesicles (BBMV) from chronically inflamed ileum. Kinetic studies demonstrated that the maximal rate of uptake of
SCFA, but not the affinity for SCFA, was reduced in chronically inflamed rabbit ileum. These data demonstrate that a distinct SCFA/HCO
3 exchange is present on BBMV
of villus but not crypt cells in normal rabbit ileum.
SCFA/HCO
3 exchange is inhibited in
chronically inflamed rabbit ileum. The mechanism of inhibition is most
likely secondary to a reduction in transporter numbers rather than
altered affinity for SCFA.
inflammatory bowel disease; short-chain fatty acid transport; immune regulation of nutrient transport; anion exchanger
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