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1 Department of Medicine, Division of Diabetes & Endocrinology, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: darleen.sandoval{at}vanderbilt.edu.
The aim of this study was to determine if activation of central type II glucocorticoid receptors can blunt autonomic nervous system (ANS) counterregulatory responses to subsequent hypoglycemia. Sixty conscious unrestrained Sprague-Dawley rats were studied during 2-day experiments. Day 1 consisted of either two episodes of clamped 2hr hyperinsulinemic (30pmol/kg/min) hypoglycemia (2.8±0.1mM; n=12; HYPO), hyperinsulinemic euglycemia (6.2±0.1mM; n=12; EUG), hyperinsulinemic euglycemia plus simultaneous lateral cerebroventricular infusion of saline (24µl/hr; SAL; n=8) or hyperinsulinemic euglycemia plus either lateral cerebral ventricular infusion (n=8; LV DEX), fourth cerebral ventricular (n=10; 4V DEX), or peripheral (n=10; P DEX) infusion of dexamethasone (5µg/h), a specific type II glucocorticoid receptor analog. For all groups, Day 2 consisted of a 2hr hyperinsulinemic (30pmol/kg/min) hypoglycemic (2.9±0.2mM) clamp. The HYPO group had blunted epinephrine, glucagon, and endogenous glucose production in response to subsequent hypoglycemia. Consequently, the glucose infusion rate to maintain the glucose levels was significanlty greater in HYPO vs. all other groups. The LV DEX group did not have blunted counterregulatory responses to subsequent hypoglycemia, but the P DEX and 4V DEX groups had significanlty lower epinephrine and norepinephrine responses to hypoglycemia compared to all other groups. In summary, peripheral and 4V, but not LV infusion of dexamethasone led to significant blunting of autonomic counterregulatory responses to subsequent hypoglycemia. These data suggest that prior activation of type II glucocorticoid receptors within the hindbrain plays a major role in blunting ANS counterregulatory responses to subsequent hypoglycemia in the concisous rat.
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