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Rapid Effects of Hydrocortisone on Glucose-induced Insulin Secretion in Healthy Humans

This study has been completed.
Information provided by:
Medical University of Vienna Identifier:
First received: July 1, 2008
Last updated: May 31, 2011
Last verified: January 2009
The purpose of this study is to investigate the effect of hydrocortisone on glucose-induced insulin secretion and sensitivity, by means of an intravenous glucose tolerance test with frequent sampling (FSIGT) followed by minimal model analysis. In a randomized single-blind cross-over design, the subjects will receive either hydrocortisone or placebo 4 minutes before an intravenous glucose load.

Condition Intervention Phase
Drug: Hydrocortisone
Drug: Glucose 33%
Phase 4

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Single Blind (Participant)
Primary Purpose: Basic Science
Official Title: Rapid Effects of Hydrocortisone on Glucose-induced Insulin Secretion in Healthy Humans

Resource links provided by NLM:

Further study details as provided by Medical University of Vienna:

Primary Outcome Measures:
  • Plasma insulin, glucose and C-peptide [ Time Frame: Minutes: -10, -5, 0, 3, 4, 5, 6, 8, 10, 15, 20, 30, 40, 60, 80, 100, 120, 150, 180 ]

Secondary Outcome Measures:
  • Plasma levels of appetite-regulatory hormones: ghrelin, PYY and nesfatin-1. [ Time Frame: Minutes: -10, 0, 30, 60, 120, 180 ]

Enrollment: 10
Study Start Date: June 2008
Study Completion Date: December 2008
Primary Completion Date: October 2008 (Final data collection date for primary outcome measure)
Intervention Details:
    Drug: Hydrocortisone
    0.6 mg/kg body weight, intravenous bolus given at time-point minus 4'
    Drug: Glucose 33%
    1ml/kg body weight, intravenous bolus given at time-point 0'
Detailed Description:

Glucocorticoids (mainly cortisol in men and corticosterone in rodents) are secreted in the adrenal cortex under the control of the hypothalamic-pituitary-adrenal (HPA) axis. They are known for and named after their combined actions on glucose metabolism: suppression of insulin secretion, inhibition of glucose uptake in peripheral tissues, and promotion of gluconeogenesis in the liver. As a result, glucose intolerance accompanies syndromes of cortisol excess, while recurrent hypoglycemia, especially in response to stress, is a typical feature of isolated familial glucocorticoid deficiency. Almost any acute severe challenge to homeostasis or stress will activate the hypothalamic-pituitary-adrenal (HPA) axis and cause a rise in plasma glucocorticoid levels, which is essential for survival. Thanks to their immunosuppressive and antiinflammatory actions, glucocorticoids are widely-used therapeuticals with important adverse effects.

The need to optimize the benefit-risk ratio of glucocorticoid therapy has lead to a recent focus of research in the pathways mediating their effects. Glucocorticoids act rapidly and within minutes, exerting effects which contradict the classical genomic signalling pathway. Little is known on the clinical rapid effects of glucocorticoids on carbohydrate metabolism. Corticosterone acutely lowers insulin plasma concentrations and their response to hyperglycemia in rodents in vivo. Intraperitoneally administered hydrocortisone suppresses the insulin levels stimulated by intravenous glucose in mice. Although subject to numerous studies, the metabolic effects of glucocorticoids have been generally tested after giving dexamethasone for a few days.

To our knowledge, there are no data on rapid effects of glucocorticoids on insulin secretion and sensitivity in humans. Despite the increased interest in rapid effects of steroids in the last decade, the immediate effects of glucocorticoids on carbohydrate metabolism have not yet been studied. This question is not easy to address in vivo because of the multiple (also compensatory) influences that can impact the endocrine pancreas. Therefore, we propose to use a rapid approach, studying the effect of a bolus of hydrocortisone on the response to an intravenous glucose tolerance test with frequent sampling (FSIGT).

The FSIGT consists in giving intravenously a glucose bolus and taking frequently blood samples afterwards for determining glucose, insulin and C-peptide. The glucose and insulin data analysed with the minimal model technique allow the calculation of the acute insulin response, glucose effectiveness and the insulin sensitivity index. The data on C-peptide will be used to evaluate the beta cell function.

The effects of Hydrocortisone on glucose-induced insulin secretion and sensitivity will be investigated by means of an FSIGT followed by minimal model analysis. The subjects will receive in a randomized single-blind cross-over design:

  1. 0.6 mg/kg body wt Hydrocortisone + 330 mg/kg body wt glucose
  2. Placebo + 330 mg/kg body wt glucose

Ages Eligible for Study:   18 Years to 60 Years   (Adult)
Sexes Eligible for Study:   Male
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

  • Healthy subjects
  • No concomitant medication
  • BMI < 25 kg/m2
  • Age: 18-60 years old

Exclusion Criteria:

  • Impaired glucose tolerance or diabetes mellitus
  • Hyperthyroidism, hypothyroidism
  • Hepatic, renal or cardiovascular diseases
  • Malignancies
  • History of medical therapy within 3 weeks prior to enrolment into the study
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Please refer to this study by its identifier: NCT00709839

Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna
Vienna, Austria, A-1090
Sponsors and Collaborators
Medical University of Vienna
Principal Investigator: Anton Luger, MD Medical University of Vienna
  More Information

Responsible Party: Prof. Dr. Anton Luger, Department of Medicine III, Medical University of Vienna Identifier: NCT00709839     History of Changes
Other Study ID Numbers: FSIGT_Hydrocortisone_01
Study First Received: July 1, 2008
Last Updated: May 31, 2011

Keywords provided by Medical University of Vienna:
carbohydrate metabolism
appetite-regulatory hormones

Additional relevant MeSH terms:
Hydrocortisone 17-butyrate 21-propionate
Cortisol succinate
Hydrocortisone acetate
Anti-Inflammatory Agents processed this record on April 25, 2017