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Gastrointestinal Research Group, Health Sciences Centre, University of Calgary, Calgary, Alberta, Canada T2N 4N1
Na+-glucose cotransporter
(SGLT1) expression and the role of actin in epidermal
growth factor (EGF)-induced alterations in glucose transport and
brush-border surface area were examined in New Zealand White rabbit
jejunal loops. In separate experiments, EGF or EGF concurrent with
cytochalasin D, an inhibitor of actin polymerization, was administered
to the experimental loop and compared with its vehicle control. SGLT1
expression was measured by Western blot in brush-border membrane
vesicles (BBMV) after 5-min and 1-h exposure. Glucose kinetics were
determined by a rapid filtration technique, and brush-border surface
area was examined by electron microscopy after 1-h exposure. The effect of cytochalasin D alone on BBMV glucose kinetics and brush-border surface area was also assessed. EGF resulted in a significant increase
in BBMV SGLT1 expression (P < 0.05),
glucose maximal uptake
(Vmax;
P < 0.001), and absorptive
brush-border surface area (P < 0.001). These effects were abolished with concurrent cytochalasin D
treatment. Cytochalasin D alone had no effect on glucose transport or
brush-border surface area. The findings suggest that EGF acutely
upregulates jejunal brush-border surface area and the
Vmax for jejunal
glucose uptake via the recruitment and insertion of SGLT1 from an
internal pool into the brush border by a mechanism that is dependent on
actin polymerization.
epidermal growth factor; sodium-glucose cotransporter; glucose transport
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