Metabolic Adaptations to Dexamethasone‐Induced Insulin Resistance in Healthy Volunteers

Nicod, Nathalie; Giusti, Vittorio; Besse, Christine; Tappy, Luc

doi:10.1038/oby.2003.90

Cited by 125Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiet, Metabolism, and Disease

Metabolic Adaptations to Dexamethasone‐Induced Insulin Resistance in Healthy Volunteers

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Nicod, Nathalie, Giusti, Vittorio, Besse, Christine, Tappy, Luc·2003·Obesity Research

DOI 10.1038/oby.2003.90

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Abstract

Objective: Insulin resistance is observed in individuals with normal glucose tolerance. This indicates that increased insulin secretion can compensate for insulin resistance and that additional defects are involved in impaired glucose tolerance or type 2 diabetes. The objective of this study was to evaluate a procedure aimed at assessing the compensatory mechanisms to insulin resistance. Research Methods and Procedures: Eight healthy nonobese female patients were studied on two occasions, before and after administration of 2 mg/d dexamethasone for 2 days during a two‐step hyperglycemic clamp. Insulin secretion was assessed from plasma insulin concentrations. Insulin sensitivity was assessed from the ratio of whole‐body glucose use (6, 6 2 H 2 glucose) to plasma insulin concentrations. This procedure is known to induce a reversible impairment of glucose tolerance and insulin resistance. Results: In all subjects, dexamethasone induced a decrease in insulin sensitivity and a proportionate increase in first‐phase insulin secretion and in insulin concentrations at both steps of glycemia. The resulting hyperinsulinemia allowed the restoration of normal whole‐body glucose uptake and the suppression of plasma free fatty acids and triglycerides. In contrast, the suppression of endogenous glucose production was impaired after dexamethasone (p < 0.01). Discussion: Increased insulin secretion fully compensates dexamethasone‐induced insulin resistance in skeletal muscle and adipose tissue but not in the liver. This suggests that failure to overcome hepatic insulin resistance can impair glucose tolerance. The compensatory insulin secretion in response to insulin resistance can be assessed by means of a hyperglycemic clamp after a dexamethasone challenge.

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Glucocorticoid-induced hyperinsulinaemia is regarded as an adaptation of pancreatic β-cell function to glucocorticoid-induced insulin resistance in liver, muscle, and adipose tissues.
“Glucocorticoid-induced hyperinsulinaemia is regarded as an adaptation of pancreatic â-cell function to the GC-induced insulin resistance in liver, muscle and adipose tissues, either through hyperglycaemia, by other signalling mechanisms, or most likely a combination of these mechanisms.27,28”
From Twenty‐four‐hour profiles of plasma glucose, insulin, C‐peptide and free fatty acid in subjects with varying degrees of glucose tolerance following short‐term, medium‐dose prednisone (20 mg/day) treatment: evidence for differing effects on insulin secretion and action (2012) · cites this paper as [28]

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Investigation of the mechanisms contributing to the compensatory increase in insulin secretion during dexamethasone-induced insulin resistance in rhesus macaques
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Authors: Nicod, N., Giusti, V., Besse, C., & Tappy, L.
Affiliations: University of Lausanne (CH)
Centre Hospitalier Universitaire Vaudois (CH)
Corresponding author: Tappy, Luc
ORCID: Tappy, Luc
Venue: Obesity Research
Publisher: Wiley
Published: 2003-05
Volume: 11
Issue: 5
Pages: 625-631
ISSN: 1071-7323 (ISSN-L)
1550-8528
DOI: 10.1038/oby.2003.90
OpenAlex: W1969834886
Cited by: 125
References: 41
Citations by year: 2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 4 · 2017: 2 · 2016: 12 · 2015: 8 · 2014: 10 · 2013: 9 · 2012: 9
FWCI: 3.52
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3416 d)
Locations: Obesity Research (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Funders: National Science Foundation
Eli Lilly and Company
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
Topics: Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords: insulin resistance, dexamethasone, compensatory insulin secretion, first-phase insulin secretion, hyperinsulinemia, hyperglycemic clamp, hepatic insulin resistance, endogenous glucose production, plasma free fatty acids, plasma triglycerides, skeletal muscle glucose uptake, adipose tissue glucose uptake, glucose tolerance, type 2 diabetes
MeSH terms: Adult, Blood Glucose, Dexamethasone, Fatty Acids, Nonesterified, Female, Glucagon, Glucocorticoids, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Triglycerides, Glucose Clamp Technique

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Metabolic Adaptations to Dexamethasone‐Induced Insulin Resistance in Healthy Volunteers

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