Inhibition of cyclic 3',5'-AMP phosphodiesterase in islet cells and other tissues by tolbutamide.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Perlman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Both cyclic AMP and a specific inducer acting in concert are required for the synthesis of many inducible enzymes in E. coli. Little enzyme is made in the absence of either. In contrast to the specific inducers which stimulate the synthesis only of the proteins required for their metabolism, cyclic AMP controls the synthesis of many proteins. Glucose and certain other carbohydrates decrease the differential rate of synthesis of inducible enzymes by lowering cyclic AMP concentrations. In the lac operon, cyclic AMP acts at the promoter site to facilitate initiation of transcription. This action requires another protein, the cyclic AMP receptor protein. The nucleotide stimulates tryptophanase synthesis at a translational level. The action of cyclic AMP in E. coli may serve as a model to understand its action on transcriptional and translational processes in eukaryotes.
A cyclic AMP binding protein has been purified over 100-fold from E. coli extracts. Protein purified from wild-type strains binds cyclic AMP with an apparent dissociation constant of 1-2 x 10(-6)M. Two mutant strains that are unresponsive to exogenous cyclic AMP have altered binding activity; the protein purified from one of these mutants has a decreased affinity for cyclic AMP (apparent dissociation constant = 2 x 10(-5)M). Extracts of this mutant are deficient in their ability to support beta-galactosidase synthesis in vitro. The addition of purified, wild-type binding protein to these extracts restores enzyme synthesis toward normal. Because this binding protein appears to be required for cyclic AMP action, we suggest it be called the cyclic AMP receptor protein (CR protein).
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Transient hyperglycemia during acute illness may represent the earliest clinical sign of impaired beta cell function. This study sought to characterize the clinical presentation of patients with stress hyperglycemia and to determine the prevalence of immunologic and endocrinologic markers associated with prediabetes. Thirty-six children were studied. They were referred to us for routine evaluation after an episode of hyperglycemia during severe intercurrent illness. Immunologic markers (insulin autoantibodies and islet cell autoantibodies) and intravenous glucose tolerance test for evaluation of first phase insulin secretion rate were performed in all participants. Islet cell autoantibodies were negative in all patients. In eight patients, the first phase insulin response was below the first percentile (46 microU/ml) at the first determination. Insulin autoantibodies were positive in another three children (> 60 nU/ml). Twelve to sixteen months later, all children were re-evaluated and all had normal results. None of the patients developed diabetes during the study (mean 3.2 years). Our data support the idea that episodes of hyperglycemia during severe illness without additional risk factors are a minimal risk factor, if any, for future development of IDDM.
Explore the source record for details and available documents.