par Balasse, Edmond 
;Couturier, Etienne ;Franckson, Jean
Référence Diabetologia, 3, 6, page (488-493)
Publication Publié, 1967-12
;Couturier, Etienne ;Franckson, Jean Référence Diabetologia, 3, 6, page (488-493)
Publication Publié, 1967-12
Article révisé par les pairs
| Résumé : | The metabolic effects of a 120 min sodium β- hydroxybutyrate infusion (5 mmoles/kg/h) were studied in healthy anaesthetized dogs. - Arterial blood sugar decreased progressively, the fall averaging 25 mg/100 ml from the 80th min onwards. A slight, transient increase in plasma insulin concentration was observed with a mean peak of + 8 μU/ml at the 10 th min of infusion. The disappearance rates of a12C-glucose load or of a tracer of14C-glucose were not modified by the sodium β- hydroxybutyrate infusion. Isotope dilution calculation showed that hypoglycaemia was entirely the consequence of a reduction in hepatic glucose output. - Plasma NEFA concentration decreased during the first hour, the fall averaging 180 μ moles/l. Subsequently, despite the maintenance of the infusion of ketone bodies, plasma NEFA returned to basal levels or above in some dogs, while remaining at low levels in others. Turnover studies using a constant infusion of14C-palmitate, revealed that the decrease in NEFA concentration was the consequence of both an inhibition of NEFA outflow from adipose tissue and an increase in the rate of NEFA uptake by the tissues. - Contrary to data of the literature, our results do not suggest that the prolonged inhibitory effect of sodium β-hydroxybutyrate on hepatic glucose output could be mediated through the minor pancreatic stimulation. This could, however, explain the NEFA changes observed. © 1967 Springer-Verlag. |
