TY - JOUR
T1 - Effect of insulin on plasma norepinephrine and 3,4-dihydroxyphenylalanine in obese men
AU - O'Hare, James A.
AU - Minaker, Kenneth L.
AU - Meneilly, Graydon S.
AU - Rowe, John W.
AU - Pallotta, Johanna A.
AU - Young, James B.
N1 - Funding Information:
Supported in part by USPHS Grant Nos. DK 20378, HL 36568, AG 00599, and RR 01032. Dr O’Hare was the recipient oflnterna-tional Research Fellowship No. FOS TWO3168 (Fogarty Foundation, National Institutes of Health) and an Ainsworth Travelling Scholarship from the University College, Cork, Ireland; Dr Men-eilly was the recipient of a Medical Research Council of Canada Fellowship.
PY - 1989/4
Y1 - 1989/4
N2 - Increasing evidence relates serum insulin level and blood pressure in obese individuals. Although the connection between these two factors is not established, a common presumption is that the sympathetic nervous system is somehow involved, in part, because laboratory studies demonstrate insulin stimulation of sympathetic and cardiovascular activity. Because the obese may exhibit altered responsiveness to insulin action, the current investigation compared cardiovascular and neurohumoral responses to euglycemic insulin infusion (200 mU/m2/min) in obese and lean men. At baseline, obese men displayed higher glucose and insulin levels, faster pulse rates, and elevated mean arterial pressures (MAP) than lean controls; plasma norepinephrine (NE) and 3,4-dihydroxyphenylalanine (DOPA) concentrations, however, did not differ. During insulin infusion, pulse rate increased equally in obese and lean subjects (from 69 to 78 min-1 in obese and from 56 to 66 min-1 in lean subjects), while MAP remained unchanged in both groups. Elevations in plasma NE (+85 pg/mL in obese and +109 in lean pg/mL) and reductions in plasma DOPA (-233 pg/mL in obese and -376 pg/mL in lean) did not differ between groups. Sodium excretory rate decreased during insulin infusion in lean subjects by 2.2 mEq/h but increased in obese by 5.3 mEq/h (difference in response between groups, P = .024). Thus, in these obese men, cardiovascular and sympathetic responses to insulin persist despite evidence of moderate insulin resistance; increased sympathetic activity, as a cause for the resting tachycardia and borderline hypertension at baseline, seems unlikely.
AB - Increasing evidence relates serum insulin level and blood pressure in obese individuals. Although the connection between these two factors is not established, a common presumption is that the sympathetic nervous system is somehow involved, in part, because laboratory studies demonstrate insulin stimulation of sympathetic and cardiovascular activity. Because the obese may exhibit altered responsiveness to insulin action, the current investigation compared cardiovascular and neurohumoral responses to euglycemic insulin infusion (200 mU/m2/min) in obese and lean men. At baseline, obese men displayed higher glucose and insulin levels, faster pulse rates, and elevated mean arterial pressures (MAP) than lean controls; plasma norepinephrine (NE) and 3,4-dihydroxyphenylalanine (DOPA) concentrations, however, did not differ. During insulin infusion, pulse rate increased equally in obese and lean subjects (from 69 to 78 min-1 in obese and from 56 to 66 min-1 in lean subjects), while MAP remained unchanged in both groups. Elevations in plasma NE (+85 pg/mL in obese and +109 in lean pg/mL) and reductions in plasma DOPA (-233 pg/mL in obese and -376 pg/mL in lean) did not differ between groups. Sodium excretory rate decreased during insulin infusion in lean subjects by 2.2 mEq/h but increased in obese by 5.3 mEq/h (difference in response between groups, P = .024). Thus, in these obese men, cardiovascular and sympathetic responses to insulin persist despite evidence of moderate insulin resistance; increased sympathetic activity, as a cause for the resting tachycardia and borderline hypertension at baseline, seems unlikely.
UR - http://www.scopus.com/inward/record.url?scp=0024583798&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0024583798&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(89)90118-2
DO - 10.1016/0026-0495(89)90118-2
M3 - Article
C2 - 2498609
AN - SCOPUS:0024583798
SN - 0026-0495
VL - 38
SP - 322
EP - 329
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 4
ER -