Abstract
Summary
Nilevar, but not testosterone, was effective in reducing the hyperglycemic response to exogenous glucagon in rats. Castrated rats were hypersensitive to the glucose elevating properties of glucagon for several days immediately after operation but by 30 days were resistant to the effects of glucagon. The refractory state induced by Nilevar probably was not mediated through the hypophysis, the hypophyseal target glands, or by blocking hepatic glycogenolytic pathways.
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