Abstract
Besides its lipogenic and lipolytic functions, adipose tissue has been recognized as an important site of lactate production by epididymal adipocytes under experimental conditions in which insulin sensitivity was increased (cold exposure) or reduced (glucose perfusion). Insulin sensitivity of adipocytes was assessed by its antilipolytic effect and its stimulation of glucose uptake. We showed that, in adipocytes isolated from control and cold-exposed animals, glycerol and lactate production rose simultaneously, in response to norepinephrine. On the other hand, in adipocytes from glucose-perfused animals, we observed a dissociation between lipolytic and glycolytic responses. Indeed, lactate production in response to norepinephrine reached 60% of maximal response (10(-7)M) while the lipolytic response was still basal. This phenomenon was the result of a desensitization of beta-adrenergic receptors. However, the sensitivity of adipocytes to stimulation of lactate production by catecholamines was not different between control and glucose-perfused rats. Because lactate production in response to norepinephrine was not affected by desensitization, it suggests that lactate production is under alpha 1-adrenergic control. We confirmed this hypothesis.
Published Version
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