Summary
Indirect evidence suggests that sulfonylureas, in addition to stimulating insulin
release, exert additional effects at extra-pancreatic levels which are of value in
the management of type 2 diabetes. In order to characterize in vivo some of these
effects, insulin sensitivity was studied in 9 type 1 diabetics with no residual insulin
secretory activity, during treatment with chlorpropamide (250 mg b.i.d. for 8 days)
and with glipizide (5 mg t.i.d. for 8 days).
Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator®), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by
the amount of glucose required to keep the blood glucose at preinfusion levels. Chlorpropamide
and glipizide administration was accompanied by a significant increase of the amount
of glucose required to clamp blood glucose levels, while serum (free) insulin levels
were superimposable during the different clamping studies. In the absence of endogenous
insulin release, these data strongly suggest that the two sulfonylureas employed enhance
in vivo the peripheral sensitivity to insulin.
Further studies are required to indicate a preferential site of action (liver, muscle,
adipose tissue) of sulfonylureas.
Key-Words:
Glucose
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Clamp
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Insulin Sensitivity
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Sulfonylureas
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Glipizide
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Chlorpropamide
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Diabetes Mellitus (Type 1)
