The stimulating effect of 3',5'-(cyclic)adenosine monophosphate and lipolytic hormones on 3-O-methylglucose transport and 45Ca2+ release in adipocytes and skeletal muscle of the rat.
(1) In order to assess the possible role of 3',5'-(cyclic)adenosine monophosphate (cAMP) in the control of glucose transport, the effect of the nucleotide or agents known to increase its intracellular concentration on sugar transport or 45Ca2+ washout were characterized in epididymal fat pads, free fat cells and soleus muscles of the rat. (2) When added to the incubation medium, cAMP (0.1-2.0 mM) stimulated 3-O-[14C]methylglucose washout from fat pads. This effect was abolished by cytochalasin B, and additive to that induced by submaximal (10-25 microU/ml), but not by supramaximal (10 microU/ml) concentrations of insulin. (3) cAMP (2 mM) stimulated the conversion of [U-14C]glucose into CO2 and triacylglycerols. This effect was additive to that of insulin (100 microU/ml). (4) ACTH, glucagon, adrenaline, noradrenaline and salbutamol, which are all known to increase the cAMP content of adipose tissue, stimulated the washout of 3-O-[14C]methylglucose and 45Ca2+ from preloaded fat pads. The fractional losses of the two isotopes were significantly correlated (P less than 0.001, r = 0.73). (5) In free fat cells, adrenaline (10(-6) M) and salbutamol (10(-5) M) stimulated the uptake of 3-O-[14C]methylglucose, and salbutamol (10(-5) M) did not interfere with the stimulating effect of insulin (25 microU/ml) on sugar uptake. (6) In rat soleus muscles, adrenaline and salbutamol produced a dose-dependent stimulation of the washout of 3-O-[14C]methylglucose and 45Ca2+. The effect of adrenaline on sugar efflux was abolished by propranolol. (7) It is concluded that the activation of the glucose transport system by insulin is unlikely to be mediated by a drop in the cellular concentration of cAMP. An increase in cAMP brought about by beta-adrenoceptor agonists or lipolytic hormones may induce a mobilization of calcium ions from cellular pools into the cytoplasm, which in turn leads to the activation of the glucose transport system demonstrated in the present as well as in several earlier studies.
D019325:3-O-Methylglucose; D000273:Adipose Tissue / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D000242:Cyclic AMP / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D005934:Glucagon / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D008757:Methylglucosides / Q000378:metabolism*; D008759:Methylglycosides / Q000378:metabolism*; D009132:Muscles / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D008757:Methylglucosides; D008759:Methylglycosides; D019325:3-O-Methylglucose; D000324:Adrenocorticotropic Hormone; D005934:Glucagon; D000242:Cyclic AMP; D000420:Albuterol; D002118:Calcium; D009638:Norepinephrine; D004837:Epinephrine