Metabolic Effects of Prolonged Sympathetic Nerve Stimulation in Canine Subcutaneous Adipose Tissue

Abstract The release of glycerol, free fatty acids (FFA), lactate, pyruvate and CO 2 as well as the uptake of glucose and O 2 was investigated in canine subcutaneous adipose tissue perfused with blood at a constant rate. Biopsy specimens were analyzed for lactate and glycogen content. Water was found to constitute 17±4 per cent of the wet weight. In unstimulated adipose tissue net glycerol release was 0.25±0.03 and net FFA release 0.12±0.06 μmoles/min/100 g adipose tissue. Both increased during sympathetic nerve stimulation for 50 min. The release of FFA and glycerol was enhanced by inhibition of adrenergic α‐receptors (dihydroergotamine 75–150 μg i.a.) and abolished by blockade of adrenergic β‐receptors (propranolol 400 μg i.a.). Basal glucose uptake averaged 1.4 μmoles/min/100 g tissue and was not significantly affected by nerve stimulation either before or after receptor blockade. The glycogen content, which averaged 3 μmoles glucose/g tissue during basal conditions, decreased by 30 per cent during sympathetic nerve stimulation, provided β‐receptors were not inhibited. During nerve stimulation lactate accumulated in adipose tissue and there was an increased net release of lactate into the blood. These effects were inhibited by either α‐ or β‐receptor blockade. During basal conditions 2.4±0.6 μmoles O 2 were extracted per min per 100 g tissue. The extraction decreased upon nerve stimulation provided α‐receptors were intact and increased if they were inhibited. The results indicate that stimulation of adrenergic β‐receptors in adipose tissue causes lipolysis and glycogenolysis and that this mobilization when combined with α‐adrenergic vasoconstriction leads to increased production and accumulation of lactate.