Dual effect of isoprenaline on glucose transport and response to insulin in isolated adipocytes.
Glucose transport as assessed by the uptake rate of 3-O-methylglucose was stimulated in isolated rat fat cells by preincubation with isoprenaline or orciprenaline. The effect was apparently mediated by beta 1-receptors, since (1) it was abolished by propranolol, (2) it closely paralleled the stimulation of lipolysis, and (3) isoprenaline was 10(2) times more potent that orciprenaline. Isoprenaline enhanced the effect of submaximal insulin concentrations as well as the basal transport rate but failed to increase the maximal effect of insulin. The stimulatory effect of isoprenaline was antagonized by adenosine deaminase which removes adenosine spontaneously released from the cells, and by bordetella toxin ( IAP) which blocks the inhibitory coupling component of adenylate cyclase. Moreover, bordetella toxin uncovered an inhibitory effect of isoprenaline on insulin stimulated glucose transport. There was no apparent correlation between the effects on glucose transport and the response of cellular cyclic AMP levels to the agents investigated. It is suggested that a step in the coupling of beta-receptors and adenylate cyclase, but not total cellular cyclic AMP levels, may mediate stimulatory as well as inhibitory effects of catecholamines on glucose transport in the adipocyte.[1]References
- Dual effect of isoprenaline on glucose transport and response to insulin in isolated adipocytes. Joost, H.G., Göke, R., Steinfelder, H.J. Biochem. Pharmacol. (1985) [Pubmed]
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