Autoantibodies against the XXXX . Dissociation of the acute effects of the antibodies from the desensitization seen with prolonged exposure.

@entity1 @entity6071 @entity8277 @entity1892 @entity413 @entity897
The effect of antibodies against the @entity8277 (anti-R) found in a @entity1 with the @entity1892 of insulin resistance and acanthosis nigricans was characterized using 3T3-L1 cultured fat cells. Anti-R acutely mimicked the action of insulin by stimulating deoxyglucose uptake. With more prolonged exposure, this insulinomimetic effect decayed, @entity413 metabolism returned to basal levels, and the cells became severely resistant to the actions of insulin. As seen with anti-R from a previous @entity1 , desensitization consisted of both a dramatic decrease in the maximal responsiveness of the cells to insulin and a shift in the dose-response curve for insulin-stimulated @entity413 oxidation. The acute and chronic effects of anti-R were then compared. The concentration of anti-R required to half-maximally inhibit insulin binding averaged more than twice that required for half-maximal stimulation of @entity897 uptake, consistent with the amount of spare receptors in 3T3-L1 cells. After prolonged exposure, the insulinomimetic activity was completely lost at all concentrations of anti-R, even at those that did not completely induce insulin resistance. Thus, loss of the insulinomimetic activity of anti-R is necessary, but not sufficient, to cause desensitization. @entity6071 was required to desensitize cells to insulin than would have been predicted on the basis of the acute inhibition of binding and the number of spare receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
