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Abstract
In the present study, we examined the effect of long-term suppression of postprandial
hyperglycemia and glycemic fluctuation in Goto-Kakizaki (GK) rats, a type 2 diabetic
animal model, by nateglinide (NG), a fast-acting hypoglycemic agent, on some measures
of neuropathy and compared the outcome with the slow-acting effect of glibenclamide
(GC). GK rats fed twice daily were given NG (50 mg/kg) or GC (1 mg/kg) orally before
each meal for 24 weeks. The dose of NG and GC was determined by the data of their
comparable suppressive effects on hyperglycemia as a total sum of glucose values after
glucose load. At the end, there was no significant influence of treatment with NG
or GC on body weight, fasting blood glucose, and glycated hemoglobin in GK rats. However,
NG treatment suppressed postprandial hyperglycemia by 50% throughout the observation
period, whereas this effect was not apparent in GC-treated rats. Delayed motor nerve
conduction velocity was normalized by NG treatment, while GC had a partial (50%) effect.
GK rats showed elevated contents of sorbitol and 3-deoxyglucosone in the sciatic nerve,
and these changes were inhibited by NG treatment. Reduced Na+/K+-adenosine triphosphatase (ATPase) activity in GK rats was not affected by either
NG or GC treatment. These results suggest that meticulous control of postprandial
hyperglycemia is essential to inhibit the development of neuropathy in type 2 diabetes.
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© 2002 Published by Elsevier Inc. All rights reserved.
