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Abstract
The role of cortisol in directing the metabolic response to a combined infusion of
glucagon, epinephrine, norepinephrine, and cortisol (stress hormones) was investigated.
Chronically catheterized, conscious fasted dogs were studied before hormone infusion
and after a 70-hour stress hormone infusion containing glucagon, epinephrine, norepinephrine,
and cortisol (n = 11) or containing all these hormones except cortisol (n = 5). Combined
stress hormone infusion increased arterial plasma glucagon, cortisol, epinephrine,
and norepinephrine approximately sixfold. Whole-body glucose production (Ra), glycogenolysis, and gluconeogenesis were assessed using tracer and arteriovenous-difference
techniques. The absence of an increase in cortisol during stress hormone infusion
attenuated the increase in arterial plasma glucose concentration and Ra (Δ 81 ± 16 v 24 ± 3 mg/dL and 1.7 ± 0.3 v 0.8 ± 0.4 mg/kg/min, respectively). However, it did not alter the increase in net
hepatic glucose output (Δ 0.7 ± 0.3 v 0.8 ± 0.4 mg/kg/min). When the increase in cortisol was absent, the increase in net hepatic gluconeogenic
precursor uptake was attenuated (Δ 0.7 ± 0.3 v 0.1 ± 0.3 mg glucose/kg/min) due to a decrease in gluconeogenic precursor levels.
The efficiency of gluconeogenesis increased to a greater extent (Δ 0.19 ± 0.07 v 0.31 ± 0.11) when cortisol was not infused. The absence of an increase in cortisol
also led to marked glycogen depletion in the liver (10 ± 4 v 55 ± 10 mg/g liver). Cortisol thus plays a pivotal role in the metabolic response
to stress hormone infusion by sustaining gluconeogenesis through a stimulatory effect
on hepatic gluconeogenic precursor supply and by maintaining hepatic glycogen availability.
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Article info
Publication history
Accepted:
November 15,
1995
Received:
April 28,
1995
Footnotes
☆Supported by National Institute of Diabetes and Digestive and Kidney Diseases Grant No. R01-DK-18243 (A.D.C.), Diabetes Research and Training Center Grant No. 2-P60-DK-20593, and a Juvenile Diabetes Foundation Career Development Award (O.P.M.).
Identification
Copyright
© 1996 Published by Elsevier Inc.
