TY - JOUR
T1 - Evidence against the hypothesis that hyperinsulinemia increases sympathetic nervous system activity in man
AU - Mitrakou, Asimina
AU - Mokan, Marian
AU - Bolli, Geremia
AU - Veneman, Thiemo
AU - Jenssen, Trond
AU - Cryer, Philip
AU - Gerich, John
N1 - Funding Information:
Supported in part by funds received from the National Institutes of Health Division of Research Resources (DRR)lGeneral Clinical Research Centers (GCRC) Grants No. 5MOI RR00056 and RROOO36, and &v Diabetes, Endocrine and Metabolic Diseases (DEMD)I National Institute of Digestive Diseases (NIDD) Grants No. 5R37 DK20411, DK27085, and DK20479. M.M. was the recipient of a mentor-based research fellowshigf rom the American Diabetes Association.
PY - 1992/2
Y1 - 1992/2
N2 - To test the hypothesis that physiologic hyperinsulinemia activates the sympathetic nervous system in humans, we measured changes in plasma norepinephrine as well as epinephrine concentrations during euglycemic hyperinsulinemic clamp experiments in which normal volunteers were infused with insulin for up to 12 hours, at rates chosen to simulate the basal and postprandial hyperinsulinemia seen in insulin-resistant states. Infusions of insulin increased plasma insulin threefold (to ∼200 pmol/L) and 15-fold (to ∼1,000 pmol/L) in simulations of fasting and postprandial hyperinsulinemia. In neither experiment did plasma norepinephrine or epinephrine change significantly. In control experiments in which saline was infused for 12 hours, plasma epinephrine increased twofold (P < .05), but plasma norepinephrine did not change. Therefore, we conclude that hyperinsulinemia of the magnitude seen in the insulin-resistant humans does not increase sympathetic nervous system activity.
AB - To test the hypothesis that physiologic hyperinsulinemia activates the sympathetic nervous system in humans, we measured changes in plasma norepinephrine as well as epinephrine concentrations during euglycemic hyperinsulinemic clamp experiments in which normal volunteers were infused with insulin for up to 12 hours, at rates chosen to simulate the basal and postprandial hyperinsulinemia seen in insulin-resistant states. Infusions of insulin increased plasma insulin threefold (to ∼200 pmol/L) and 15-fold (to ∼1,000 pmol/L) in simulations of fasting and postprandial hyperinsulinemia. In neither experiment did plasma norepinephrine or epinephrine change significantly. In control experiments in which saline was infused for 12 hours, plasma epinephrine increased twofold (P < .05), but plasma norepinephrine did not change. Therefore, we conclude that hyperinsulinemia of the magnitude seen in the insulin-resistant humans does not increase sympathetic nervous system activity.
UR - http://www.scopus.com/inward/record.url?scp=0026515392&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(92)90153-2
DO - 10.1016/0026-0495(92)90153-2
M3 - Article
C2 - 1736043
AN - SCOPUS:0026515392
SN - 0026-0495
VL - 41
SP - 198
EP - 200
JO - Metabolism
JF - Metabolism
IS - 2
ER -