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G Faintrenie and A Geloen
Laboratoire de Thermoregulation et Energetique de l'Exercice, Lyon, France.
The production of lactate from glucose and lactate release have recently been recognized as a novel function of adipose tissue. It has been demonstrated that catecholamines are able to induce lactate production; nevertheless, the adrenoceptor subtype involved has not yet been clearly identified. We studied the adrenergic regulation of lactate production by epididymal adipocytes. We showed that lactate production was enhanced by noradrenaline (a nonselective adrenergic agonist) and phenylephrine (an alpha-1 adrenergic agonist). On the other hand, isoproterenol (a nonselective beta agonist) and UK 14304 (an alpha-2-adrenergic agonist) did not stimulate glycolysis. Moreover, we observed that the maximal glycolysis induced by 10(-7) M phenylephrine was not significantly different from the maximal lactate production induced by 10(-5) M norepinephrine (0.43 +/- 0.03 vs. 0.39 micromol lactate/10(6) cells. 15 min.). The sensitivity of adipocytes to glycolytic stimulation by catecholamines was much higher for phenylephrine (pD2 = 9.66 +/- 2.30) than for norepinephrine (pD2 = 7.35 +/- 0.113, P < .05). Finally, the stimulation of lactate production by norepinephrine was totally inhibited by the presence of prazosin (10(- 6)M) in the incubation medium. Our findings suggest that lactate production by epididymal adipocytes is under the control of alpha-1 adrenoceptors.
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