par Calderon-Attas, Piedad;Furnelle, Jacques 
;Christophe, Jean
Référence Biochimica et biophysica acta, 620, 3, page (387-399)
Publication Publié, 1980
;Christophe, Jean Référence Biochimica et biophysica acta, 620, 3, page (387-399)
Publication Publié, 1980
Article révisé par les pairs
| Résumé : | 1. Ethanol provoked no effect on basal and carbamylcholine-stimulated secretion of amylase from rat pancreatic fragments incubated for 1 h. 2. Ethanol enhanced in vitro synthesis of fatty acids from [1-14C]acetate and from 3H2O by 110 and 166%, respectively. The spectrum of fatty acids labelled with [1-14C]acetate in the presence of ethanol pointed to a stimulation of the malonic acid pathway, whereas the elongation of polyenoic fatty acids was unaltered. The in vitro metabolism of [1-14C]ethanol indicates that ethanol itself contributed carbon atoms to lipogenesis dose-dependently. 3. The conversion of [U-14C]glucose into sn-glycero 3-phosphate and the esterification of fatty acids into phosphatidic acids and triacylglycerols was stimulated whereas net lipolysis was unaffected. The oxidation of [U-14C]-glucose and of [1-14C]acetate to 14CO2 and the beta-oxidation of [1-14C]palmitate was reduced by 24--26%. 4. Maximal effects were produced by a 100--200 mM ethanol concentration and the concentration of ethanol evoking a similar half-maximal alteration of most processes was 20--30 mM. A 10--20 min lag period was required for the full development of these effects. 5. It is concluded that ethanol at low concentration alters the redox state of pancreatic fragments therefore favoring de novo lipogenesis and triacylglycerol formation and depressing glucose uptake and fatty acid oxidation. |
