title: Insulin-stimulated glucose transport is dependent on Golgi function in isolated working rat heart.
abstract: Insulin and epinephrine stimulate glucose uptake through distinct mechanisms. We tested the hypothesis that the golgi apparatus is involved in insulin-stimulated but not epinephrine-stimulated glucose transport and phosphorylation.
  
  
  METHODS
  We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-(3)H]glucose (5 mmol/l, 0.05 microCi/ml) and Na-oleate (0.4 mmol/l). In the absence or presence of the inhibitor of golgi function, brefeldin A (30 micromol/l), either insulin (1 mU/ml), epinephrine (1 micromol/l), or phenylephrine (100 micromol/l) plus propranolol (10 micromol/l, selective alpha -adrenergic stimulation) were added to the perfusate.
  
  
  RESULTS
  Cardiac power was stable in all groups (between 8.56+/-0.61 and 10.4+/-1.11 mW) and increased (34%) with addition of epinephrine, but not with selective alpha -adrenergic stimulation. Insulin, epinephrine, and selective alpha -receptor stimulation increased glucose transport and phosphorylation (micromol/min/g dry wt, basal: 1.19+/-0.13, insulin: 3.89+/-0.36, epinephrine: 3.46+/-0.27, alpha -stimulation: 4.08+/-0.40). Brefeldin A increased basal glucose transport and phosphorylation and blunted insulin-stimulated but not epinephrine-stimulated glucose transport and phosphorylation. Selective alpha -stimulated glucose transport and phosphorylation was also blunted by brefeldin A.
  
  
  CONCLUSIONS
  Both insulin and alpha -adrenergic stimulation result in glucose transporter translocation from a pool that requires golgi function. Stimulation with epinephrine results in glucose transporter translocation from a pool that does not require golgi function. The stimulating effects of the alpha -adrenergic pathway on glucose transport and phosphorylation are independent of changes in cardiac performance.
authors.affiliation: Department of Medicine, University of Texas-Houston Medical School, Houston, TX 77030, USA.
authors.forename: T
authors.initials: T
authors.lastname: Doenst
authors.forename: A M
authors.initials: AM
authors.lastname: Cedars
authors.forename: H
authors.initials: H
authors.lastname: Taegtmeyer
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D000935:Antifungal Agents / Q000494:pharmacology; D001692:Biological Transport; D020126:Brefeldin A / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism* / Q000493:pharmacokinetics; D006003:Glycogen / Q000378:metabolism; D006056:Golgi Apparatus / Q000378:metabolism*; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D013997:Time Factors
chemical_list: D000316:Adrenergic alpha-Agonists; D000935:Antifungal Agents; D007328:Insulin; D020126:Brefeldin A; D006003:Glycogen; D005947:Glucose; D004837:Epinephrine