TY - JOUR
T1 - The relationship of epinephrine excretion to serum lipid levels
T2 - The normative aging study
AU - Ward, Kenneth D.
AU - Sparrow, David
AU - Landsberg, Lewis
AU - Young, James B.
AU - Vokonas, Pantel S.
AU - Weiss, Scott T.
N1 - Funding Information:
Supported bv Grants No. HL-37871 and HL-4.5089 from the National Heart, Lung and Blood Institute, Grant No. MO1 RR01032 from the General Clinical Research Center, Beth Israel Hospital, and the Health Services Research and Development Senice of the Deparr-ment of Veterans .4ffairs.
PY - 1994/4
Y1 - 1994/4
N2 - Catecholamines are known to stimulate lipolysis of triglyceride stores in adipose tissue. However, the relationship of sympathoadrenal activity to serum lipid and lipoprotein concentrations remains uncertain. Since obesity, particularly the centripetal form, has recently been shown to be associated with increased urinary excretion of norepinephrine and decreased excretion of epinephrine, the possibility that the sympathoadrenal system is involved in the lipid abnormalities associated with the centripetal form of obesity was investigated. The relationship between 24-hour urinary catecholamine excretion and serum lipid and lipoprotein levels was examined among 615 male participants of the Normative Aging Study. Epinephrine excretion was positively correlated with the high-density lipoprotein cholesterol (HDL-C) level and the ratio of HDL-C to low-density lipoprotein cholesterol ([LDL-C] r = .15, P = .0002, and r = .11, P = .007, respectively) and inversely correlated with the triglyceride level (r = -.14, P = .0005). These relationships remained significant after adjusting for the effects of age, smoking, alcohol intake, adiposity, and insulin level. Epinephrine excretion was not significantly related to levels of total cholesterol or LDL-C. Norepinephrine and dopamine excretion were not significantly related to any lipid variable. These data suggest that (1) epinephrine plays an important role in regulating lipid and lipoprotein metabolism in humans, and (2) decreased adrenal medullary activity may contribute to the dyslipidemia (increased triglycerides and decreased HDL-C) commonly observed among the obese. The sympathoadrenal system therefore, along with hyperinsulinemia, may contribute to the increased cardiovascular risk associated with the insulin resistance syndrome.
AB - Catecholamines are known to stimulate lipolysis of triglyceride stores in adipose tissue. However, the relationship of sympathoadrenal activity to serum lipid and lipoprotein concentrations remains uncertain. Since obesity, particularly the centripetal form, has recently been shown to be associated with increased urinary excretion of norepinephrine and decreased excretion of epinephrine, the possibility that the sympathoadrenal system is involved in the lipid abnormalities associated with the centripetal form of obesity was investigated. The relationship between 24-hour urinary catecholamine excretion and serum lipid and lipoprotein levels was examined among 615 male participants of the Normative Aging Study. Epinephrine excretion was positively correlated with the high-density lipoprotein cholesterol (HDL-C) level and the ratio of HDL-C to low-density lipoprotein cholesterol ([LDL-C] r = .15, P = .0002, and r = .11, P = .007, respectively) and inversely correlated with the triglyceride level (r = -.14, P = .0005). These relationships remained significant after adjusting for the effects of age, smoking, alcohol intake, adiposity, and insulin level. Epinephrine excretion was not significantly related to levels of total cholesterol or LDL-C. Norepinephrine and dopamine excretion were not significantly related to any lipid variable. These data suggest that (1) epinephrine plays an important role in regulating lipid and lipoprotein metabolism in humans, and (2) decreased adrenal medullary activity may contribute to the dyslipidemia (increased triglycerides and decreased HDL-C) commonly observed among the obese. The sympathoadrenal system therefore, along with hyperinsulinemia, may contribute to the increased cardiovascular risk associated with the insulin resistance syndrome.
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U2 - 10.1016/0026-0495(94)90085-X
DO - 10.1016/0026-0495(94)90085-X
M3 - Article
C2 - 8159112
AN - SCOPUS:0028314620
SN - 0026-0495
VL - 43
SP - 509
EP - 513
JO - Metabolism
JF - Metabolism
IS - 4
ER -