Abstract

We examined the effect of acute discontinuation of an epinephrine (EPI) infusion on hepatic glucose metabolism during stress hormone infusion (SHI). Glucose metabolism was assessed in 11 conscious, 20-hour fasted dogs using tracer and arteriovenous techniques after a 3-day exposure to SHI. SHI increased EPI, norepinephrine, cortisol, and glucagon levels (∼sixfold to 10-fold), which led to marked hyperglycemia, hyperinsulinemia, and accelerated glucose metabolism. On day 3, EPI infusion was acutely discontinued for 180 minutes in five dogs while infusion of the other hormones was continued (SHI — EPI). In the remaining six dogs, all hormones were continued for the duration of the study (SHI + EPI). In SHI — EPI, EPI levels decreased from 1,678 ± 191 to 161 ± 47 pg/mL. Isoglycemia (183 ± 10 to 185 ± 15 mg/dL) was maintained with an exogenous glucose infusion. Arterial insulin levels increased from 41 ± 8 to 64 ± 8 μU/mL. Whole-body glucose utilization increased from 3.5 ± 0.5 to 9.4 ± 1.9 mg/kg/min. Nonesterified fatty acids ([NEFAs] 763 ± 292 to 147 ± 32 μmol/L) decreased. Net hepatic glucose output decreased (2.6 ± 0.6 to 0.1 ± 0.3 mg/kg/min). In SHI + EPI, hepatic glucose metabolism remained unaltered. In summary, EPI plays a pivotal role during SHI by stimulating glucose production and inhibiting glucose utilization. In part, these effects are mediated by restraining pancreatic insulin secretion.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.