Adipocyte beta-adrenoceptor sensitivity influences plasma lipid levels.

Catecholamine stimulation of lipolysis through adipocyte beta-adrenoceptors is of major importance for the regulation of lipid mobilization from adipose tissue. The influence of adipocyte beta-receptor sensitivity as assessed by an isoprenaline bioassay on circulating lipid levels was investigated in 46 healthy and drug-free subjects. beta-Receptor sensitivity was inversely related to total plasma triglycerides (r = -.62), very low density lipoprotein cholesterol (VLDL-C) (r = -.56), VLDL triglycerides (r = -.52), and apolipoprotein B (r = -.41). These relationships remained significant after adjustment for age, sex, body mass index, waist/hip ratio, fat cell volume, and circulating levels of insulin, noradrenaline, and adrenaline. beta-Receptor sensitivity accounted for 40% of the variance in total plasma triglycerides. beta-Receptor subtype sensitivity and binding capacity were also determined in fat cells using terbutaline (beta 2) and dobutamine (beta 1) bioassays and radioligand binding. Multiple regression analysis revealed that terbutaline sensitivity correlated inversely with total plasma triglycerides, apolipoprotein B, VLDL-C, and VLDL triglycerides (partial r from -.56 to -.42), but there was no correlation between dobutamine sensitivity and blood lipids (partial r from .05 to .18) or between receptor binding and blood lipids (partial r from .01 to .28). Thus, the lipolytic beta-receptor sensitivity in fat cells appears to play a hitherto-unrecognized role for lipoprotein metabolism, in particular that of VLDL. This relationship is receptor-subtype specific, particularly involving beta 2-receptors, and seems to be localized to a postreceptor step in lipolysis regulation. Low sensitivity may be of importance for the development of hypertriglyceridemia.