<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Diabetes in humans and in experimental animals
produces changes in the function and structure of the
small intestine. The authors determined the activity of
intestinal disaccharidases (maltase and sucrase) and of
6-phosphofructo-1-kinase (PFK-1) in enterocytes isolated
from the small intestine of male Wistar rats (2.5 to 3 months
old) with experimental nonobese type 2 diabetes, induced by
streptozotocin (STZ) injection on the day of birth (n0-STZ)
or on the 5th day of life (n5-STZ), with different degrees
of hyperglycemia and insulinemia (n0-STZ and n5-STZ
models). The glycemia (mmol/L) of the diabetic rats
(n0-STZ: 8.77 ± 0.47; n5-STZ: 20.83 ± 0.63) was higher
(<italic>P</italic> &lt; .01) than that of the nondiabetic (ND) rats
(5.99 ± 0.63); on the contrary, the insulinemia (ng/mL) was
significantly lower in both n0-STZ (1.74 ± 0.53; <italic>P</italic> &lt; .05)
and n5-STZ (1.12 ± 0.44; <italic>P</italic> &lt; .01) diabetic rats than in normal
rats (3.77 ± 0.22). The sucrase and maltase activities
(U/g protein) in diabetic rats (n0-STZ: 89 ± 9 and 266 ± 12;
n5-STZ: 142 ± 23 and 451 ± 57) were significantly higher
than those in the ND group (66 ± 5 and 228 ± 22). The
PFK-1 activities (mU/mg protein) in the diabetic models
(n0-STZ: 14.89 ± 1.51; n5-STZ: 13.35 ± 3.12) were significantly
lower (<italic>P</italic> &lt; .05) than in ND rats (20.54 ± 2.83). The
data demonstrated enzymatic alterations in enterocytes isolated
fromthe small intestine of n0-STZ rats that are greater
(<italic>P</italic> &lt; .05) than in the more hyperglycemic and hypoinsulinemic
n5-STZ animals. The results also show that nonobese type 2–like diabetes in the rat produces modifications that
favor an increase in glucose absorption rates.</p>
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Exp Diabesity Res. 2003; 4(2):119-123