Cited by 100Adrenal Hormones and DisordersPancreatic function and diabetesStress Responses and Cortisol

Effects of chronic elevation in plasma cortisol on hepatic carbohydrate metabolism

Goldstein, R. E., Wasserman, D. H., McGuinness, O. P., Lacy, D. B., Cherrington, A. D., Abumrad, N. N.·1993·American Journal of Physiology-Endocrinology and Metabolism

Abstract

This study was undertaken to investigate the effects of chronic physiological elevations in plasma cortisol on glycogenolysis and gluconeogenesis in conscious, overnight-fasted dogs. Experiments consisted of an 80-min tracer and dye equilibration period and a 40-min sampling period. Infusions of D-[3-3H]glucose, L-[U-14C]alanine, and indocyanine green dye were used to assess glucose production (Ra) and gluconeogenesis using tracer and arteriovenous (a-v) difference techniques. In the cortisol group, (n = 10), a continuous infusion of hydrocortisone (3.5 micrograms.kg-1 x min-1) was begun 5 days before the experiment and continued throughout the sampling period. In the saline group (n = 10), there was no infusion of cortisol. The fivefold elevation in plasma cortisol increased plasma insulin from 12 +/- 2 to 19 +/- 2 microU/ml. Glucose Ra was elevated in the cortisol group (3.5 +/- 0.2 vs. 2.8 +/- 0.2 mg.kg-1 x min-1) but net hepatic glucose output was markedly diminished (1.2 +/- 0.4 vs. 2.7 +/- 0.3 mg.kg-1 x min-1). Gluconeogenic conversion of alanine to glucose was increased slightly by cortisol (0.60 +/- 0.13 to 0.99 +/- 0.12 mumol.kg-1 x min-1), but the gluconeogenic efficiency of the liver was unchanged. Cortisol increased hepatic glycogen content evident at the end of the study greater than twofold (76.4 +/- 7.9 vs. 30.0 +/- 4.7 g/liver). These results suggest that cortisol 1) promotes glucose cycling through glycogen, 2) greatly inhibits nonhepatic glucose utilization, 3) increases hepatic gluconeogenesis in vivo primarily through enhanced substrate delivery to the liver, and 4) raises plasma insulin levels, which restrains intrahepatic gluconeogenesis.

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Crossref · 10.1152/ajpendo.1993.264.1.e119

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Authors
Goldstein, R. E., Wasserman, D. H., McGuinness, O. P., Lacy, D. B., Cherrington, A. D., & Abumrad, N. N.
Affiliations
Vanderbilt University (US)
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
1993-01-01
Volume
264
Issue
1
Pages
E119-E127
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2290181424
Cited by
100
References
27
Citations by year
2026: 1 · 2024: 4 · 2023: 2 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 3 · 2016: 1 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 2
FWCI
0.60
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01dk030515-07, 5p60dk020593-31)
  • National Institute of Diabetes and Digestive and Kidney Diseases (2-RO1-DK-30515, 5P60 DK-20593, 5RO1-DK-18243, R01DK018243)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
cortisol, hepatic glucose production, gluconeogenesis, glycogenolysis, liver glycogen, plasma insulin, dogs
MeSH terms
Alanine, Animals, Arteries, Blood Glucose, Dogs, Female, Gluconeogenesis, Glucose, Glycerol, Glycogen, Hydrocortisone, Hydroxybutyrates, Lactates, Liver, Male, Osmolar Concentration, Time Factors, Lactic Acid, 3-Hydroxybutyric Acid, Carbohydrate Metabolism

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