Importance of beta‐adrenoceptor function in fat cells for lipid mobilization

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Abstract
The role of peripheral catecholamine sensitivity in lipid mobilization was investigated in 78 healthy non‐obese subjects by comparing beta‐adre‐nergic regulation of lipolysis in isolated adipocytes with circulating catecholamines and glycerol (lipolysis index). Small intra‐individual variations (5–7%) in adipocyte lipolytic beta‐adrenoceptor sensitivity (ED50) for isoprenaline were found. However, large inter‐individual variations (almost 105‐fold) in isoprenaline ED50 were observed in abdominal or gluteal adipocytes, which correlated (r = ‐0.52) negatively with the resting plasma noradrenaline levels. A correlation was also observed between circulating noradrenaline and adipocyte ED50 for noradrenaline (r= ‐0.38). In subjects with high (ED50 < 10‐1 mol 1‐1) as compared to low isoprenaline sensitivity (ED50 > 10‐10 mol 1‐1) physical exercise induced a two times greater increase in plasma glycerol (P < 0.01), in spite of a 50% less marked increase of plasma noradrenaline (P < 0.01). Findings with beta‐adrenoceptor mRNA and with total beta‐adrenoceptor number or affinity for agonist did not show any strong correlation with the resting plasma noradrenaline level (r<0.25). In conclusion, inter‐individual variations in beta‐adrenoceptor sensitivity and its relation to circulating noradrenaline can be ascribed to specific modulations of either BAR‐subtypes or in the postreceptor activation of lipolysis. These variations in adipocyte beta‐adrenoceptor sensitivity may participate in the regulation of peripheral nervous activity and play a putative role in lipolysis during exercise when subjects with high beta‐adrenoceptor sensitivity increased their ability to mobilize lipids despite a reduced noradrenaline response.