Trial reportThe Journal of clinical endocrinology and metabolism2015
Glucocorticoid Excess Increases Hepatic 11β-HSD-1 Activity in Humans: Implications in Steroid-Induced Diabetes.
Trial report in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Upregulation of hepatic flavin-containing monooxygenase 3 by increased corticosterone via glucocorticoid receptor contributes to gestational diabetes mellitus.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Medications and medical costs for diabetes patients with or without chronic respiratory disease in Beijing, China: A retrospective study.Frontiers in endocrinology · 2022Observational
- The Role of Very Low Calorie Ketogenic Diet in Sympathetic Activation through Cortisol Secretion in Male Obese Population.Journal of clinical medicine · 2021Article
- Drugs Affecting Body Weight, Body Fat Distribution, and Metabolic Function-Mechanisms and Possible Therapeutic or Preventive Measures: an Update.Current obesity reports · 2021Review
- Glucose metabolism in Cushing's syndrome.Current opinion in endocrinology, diabetes, and obesity · 2020Review
- Glucocorticoids regulate AKR1D1 activity in human liver in vitro and in vivo.The Journal of endocrinology · 2020Article
- Article
- Stress and Obesity: Are There More Susceptible Individuals?Current obesity reports · 2018Review
- Drug-induced obesity and its metabolic consequences: a review with a focus on mechanisms and possible therapeutic options.Journal of endocrinological investigation · 2017Review
- A Rare Case of Apparent Mineralocorticoid Excess Presenting as Endocrine Hypertension.Indian journal of nephrologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
contextAnimal studies indicate that glucocorticoids increase hepatic 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) expression and activity.
objectiveOur goal was to determine whether glucocorticoid excess increases cortisol production in the liver via 11β-HSD-1 enzyme pathway in humans.
designA total of 1 mg each [4-(13)C] cortisone and [9,12,12-(2)H3] cortisol were ingested, and [1,2,6,7-(3)H] cortisol was infused to measure C13 cortisol (derived from ingested [4-(13)C] cortisone) turnover using the triple tracer technique, whereas glucose turnover was measured using isotope dilution technique following [6-6(2)H2] glucose infusion during a saline clamp.
settingThis study took place at the Mayo Clinic Clinical Research Unit.
participantsThirty nondiabetic healthy subjects participated.
interventionSubjects were randomized to hydrocortisone (n = 15) or placebo 50 mg twice daily (n = 15) for 1 week. OUTCOME MEASURES: Hepatic cortisol production and endogenous glucose production were measured.
resultsPlasma cortisol concentrations were higher throughout the study period in hydrocortisone group. Rates of appearance of C13 cortisol and hepatic C13 cortisol production were higher in hydrocortisone vs placebo group, indicating increased hepatic 11β-HSD-1 activity. Higher plasma cortisol and presumably higher intrahepatic cortisol was associated with impaired suppression of endogenous glucose production in hydrocortisone vs placebo group.
conclusionChronic glucocorticoid excess increases intrahepatic cortisone to cortisol conversion via the 11β-HSD-1 pathway. The extent to which this causes or exacerbates steroid induced hepatic insulin resistance remains to be determined.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.