Abstract
The defect in catecholamine-stimulated adenylate cyclase which is characteristic of the ob/ob mouse apparently is associated with a decrease in the sensitivity of the system to guanine nucleotides (guanosine 5''-[.beta..gamma.-imido]triphosphate and GTP). No difference in the .beta.-adrenergic receptor activity was found between the lean and obese mice on the basis of their capacity to bind the .beta.-adrenergic antagonist [3H]dihydroalprenolol. A defect in the activation of the adenylate cyclase by .beta.-adrenergic agents may reside in the guanyl nucleotide binding site(s).