Adrenergic responsiveness of adipose tissue lipolysis in autonomic failure.

Abstract

The sympathetic nervous system mobilizes lipids from adipose tissue through stimulation of beta-adrenergic receptors. The increase in lipid supply augments lipid oxidation. Patients with autonomic failure provide a unique opportunity to further elucidate the role of the adrenergic system in adipose tissue metabolism. In 4 patients with severe pure autonomic failure (PAF), in 3 multiple system atrophy patients (MSA), and in 16 healthy young controls, we inserted a microdialysis catheter in abdominal adipose tissue. The catheter was perfused with incremental concentrations of the nonselective beta-adrenoreceptor agonist isoproterenol. Dialysate glucose, lactate, and glycerol were measured to assess glucose supply, glycolysis, and lipolysis, respectively. Basal dialysate glycerol concentrations were 84 +/- 28 microM in PAF and 130 +/- 64 microM in MSA patients. The increase in dialysate glycerol with isoproterenol was identical in PAF and in MSA patients. We found an almost complete overlap in dialysate glycerol concentrations during isoproterenol stimulation between PAF and MSA patients and healthy young control subjects. Our findings suggest that adipose tissue metabolism is remarkably well preserved in patients with chronic sympathetic denervation, both at rest and during local adrenergic stimulation. We propose that beta-adrenoreceptor upregulation is compensated by a desensitization of post receptor mechanisms or by an upregulation of antilipolytic pathways.