Catecholamine regulation of local lactate production in vivo in skeletal muscle and adipose tissue: role of -adrenoreceptor subtypes.
CONTEXT: The regulation of lactate production in skeletal muscle (SM) and adipose tissue (AT) is not fully elucidated. OBJECTIVE: Our objective was to investigate the catecholamine-mediated regulation of lactate production and blood flow in SM and AT in healthy, normal-weight subjects by using microdialysis. METHODS: First, lactate levels in SM and AT were measured during an iv norepinephrine infusion (n = 11). Local blood flow was determined with the 133Xe-clearance technique. Second, muscle lactate was measured during hypoglycemia and endogenous epinephrine stimulation (n = 12). Third, SM was perfused with selective beta(1-3)-adrenoreceptor agonists in situ (n = 8). Local blood flow was measured with the ethanol perfusion technique. RESULTS: In response to iv norepinephrine, the fractional release of lactate (difference between tissue and arterial lactate) increased by 40% in SM (P = 0.001), whereas remaining unchanged in AT. Blood flow decreased by 40% in SM (P < 0.005) and increased by 50% in AT (P < 0.05). In response to hypoglycemia, epinephrine increased 10-fold, and the fractional release of lactate in SM doubled (P < 0.0001). The blood flow remained unchanged. The beta2-agonist, terbutaline, caused a marked concentration-dependent increase of muscle lactate and blood flow (P < 0.0001). The beta(1)-agonist, dobutamine, induced a discrete increase of muscle lactate (P < 0.0001), and the blood flow remained unchanged. The beta3-agonist, CPG 12177, did not affect muscle lactate or blood flow. CONCLUSIONS: Catecholamines stimulate lactate production in SM, but not in AT. In SM, the beta2-adrenoreceptor is the most important beta-adrenergic receptor subtype in the regulation of lactate production.[1]References
- Catecholamine regulation of local lactate production in vivo in skeletal muscle and adipose tissue: role of -adrenoreceptor subtypes. Qvisth, V., Hagström-Toft, E., Enoksson, S., Bolinder, J. J. Clin. Endocrinol. Metab. (2008) [Pubmed]
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