Noradrenaline stimulates glucose transport in rat brown adipocytes by activating thermogenesis. Evidence that fatty acid activation of mitochondrial respiration enhances glucose transport
| Autor: | L J Bukowiecki, André Marette |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
Cholera Toxin medicine.medical_specialty Cellular respiration Lipolysis medicine.medical_treatment Palmitic Acid Biological Transport Active Palmitic Acids Biology Biochemistry Palmitic acid Norepinephrine chemistry.chemical_compound Oxygen Consumption Adipose Tissue Brown 1-Methyl-3-isobutylxanthine Internal medicine Respiration medicine Animals Hypoglycemic Agents Carnitine Molecular Biology Cytochalasin B Cells Cultured chemistry.chemical_classification Insulin Fatty Acids Glucose transporter Fatty acid Rats Inbred Strains Cell Biology Propranolol Mitochondria Rats Glucose Endocrinology Bucladesine chemistry Epoxy Compounds Body Temperature Regulation Research Article medicine.drug |
| Zdroj: | Biochemical Journal. 277:119-124 |
| ISSN: | 1470-8728 0264-6021 |
| DOI: | 10.1042/bj2770119 |
| Popis: | The mechanisms by which noradrenaline, lipolytic agents and long-chain fatty acids stimulate glucose transport were investigated in rat brown adipocytes. Glucose transport was evaluated with tracer D-[U-14C]glucose and cell respiration was measured polarographically. Noradrenaline increased basal oxygen consumption (8-10-fold) and glucose transport (4-5-fold) in a dose-dependent manner, with a maximal stimulation at 100 nM. The stimulatory effects of noradrenaline on respiration and glucose transport were selectively mimicked by dibutyryl cyclic AMP (DBcAMP), 3-isobutyl-1-methylxanthine, cholera toxin and physiological concentrations of palmitic acid. Cytochalasin B completely blocked the effects of these agents on glucose transport. The beta-adrenergic antagonist propranolol inhibited noradrenaline-induced glucose transport, but did not affect the action of DBcAMP, palmitic acid or cholera toxin on this process. The specific inhibitor of mitochondrial carnitine palmitoyltransferase, 2-tetradecylglycidic acid (McN 3802) (50 microM), inhibited the stimulatory effects of noradrenaline (100 nM) and palmitic acid (0.5 mM) on both glucose transport and mitochondrial respiration. Significantly, McN 3802 failed to affect insulin (1 nM) action under identical experimental conditions. These results demonstrate that (a) the stimulatory effects of noradrenaline on brown-adipocyte respiration and glucose transport can be dissociated from those induced by insulin, and (b) noradrenaline increases glucose transport indirectly, by activating adenylate cyclase via beta-adrenergic pathways and by stimulating mitochondrial oxidation of fatty acids. |
| Databáze: | OpenAIRE |
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