Cited by 76Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsAdrenal Hormones and Disorders

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The effect of cortisol on glucose/glucose-6-phosphate cycle activity and insulin action.

Rooney, D P, Neely, R D, Cullen, C, Ennis, C N, Sheridan, B, Atkinson, A B, Trimble, E R, Bell, P M·1993·The Journal of Clinical Endocrinology & Metabolism

DOI 10.1210/jcem.77.5.8077310

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Abstract

Increased glucose/glucose-6-phosphate (G/G6P) substrate cycle activity may be an early marker of disordered hepatic glucose metabolism. To investigate the effects of glucocorticoids on G/G6P cycle activity and insulin resistance, we studied eight normal subjects using the euglycemic glucose clamp technique with high pressure liquid chromatography-purified [2(3)H]- and [6-3H]glucose tracers at insulin infusion rates of 0.4 and 2.0 mU/kg.min after 24-h cortisol (2 micrograms/kg.min) and saline infusions. Endogenous glucose production ([6-3H]glucose) was greater after cortisol than saline in the postabsorptive state (13.3 +/- 0.5 vs. 12.2 +/- 0.5 mumol/kg.min; P < 0.05) and during 0.4-mU insulin infusion (10.5 +/- 0.7 vs. 5.0 +/- 0.8 mumol/kg.min; P < 0.005). During 2.0-mU insulin infusion, endogenous glucose production was suppressed similarly (5.1 +/- 0.4 vs. 4.1 +/- 0.5 mumol/kg.min), but glucose disappearance was less after cortisol than saline (38.7 +/- 3.5 vs. 64.6 +/- 4.3 mumol/kg.min; P < 0.001). G/G6P cycle activity after cortisol and saline was similar in the postabsorptive state and during 0.4 mU insulin. During 2.0 mU insulin, cycle activity was greater after cortisol than saline (3.6 +/- 0.9 vs. 0.8 +/- 0.5 mumol/kg.min; P < 0.005). In conclusion, cortisol induces hepatic insulin resistance without significantly changing G/G6P cycle activity. At high glucose turnover rates, G/G6P cycle activity is increased by cortisol; however, reduced glucose disappearance is the main cause of impaired insulin action.

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Authors: Rooney, D. P., Neely, R. D., Cullen, C., Ennis, C. N., Sheridan, B., Atkinson, A. B., Trimble, E. R., & Bell, P. M.
Affiliations: Royal Victoria Hospital (GB)
ORCID: Neely, R D
Venue: The Journal of Clinical Endocrinology & Metabolism
Publisher: The Endocrine Society
Published: 1993-11
Volume: 77
Issue: 5
Pages: 1180-1183
ISSN: 0021-972X (ISSN-L)
1945-7197
DOI: 10.1210/jcem.77.5.8077310
OpenAlex: W1990313681
Cited by: 76
References: 0
Citations by year: 2025: 3 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 5 · 2016: 3 · 2014: 2 · 2013: 5 · 2012: 2
FWCI: 2.18
Type: journal article
Language: en
Open access: closed
Locations: The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords: cortisol, glucocorticoids, hepatic insulin resistance, hepatic glucose metabolism, endogenous glucose production, glucose disappearance, insulin action
MeSH terms: Absorption, Adult, Blood Glucose, Female, Glucose, Glucosephosphates, Humans, Hydrocortisone, Insulin, Male, Glucose Clamp Technique, Glucose-6-Phosphate

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The effect of cortisol on glucose/glucose-6-phosphate cycle activity and insulin action.

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