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Cited by 115Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiet, Metabolism, and Disease

Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients

Alford, F., Beck-Nielsen, H., Ward, G. M., Henriksen, J. E.·1997·Diabetologia
DOI 10.1007/s001250050847
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Abstract

We tested the hypothesis that glucose intolerance develops in genetically prone subjects when exogenous insulin resistance is induced by dexamethasone (dex) and investigated whether the steroid-induced glucose intolerance is due to impairment of beta-cell function alone and/or insulin resistance. Oral glucose tolerance (OGTT) and intravenous glucose tolerance tests with minimal model analysis were performed before and following 5 days of dex treatment (4 mg/day) in 20 relatives of non-insulin-dependent diabetic (NIDDM) patients and in 20 matched control subjects (age: 29.6 +/- 1.7 vs 29.6 +/- 1.6 years, BMI: 25.1 +/- 1.0 vs 25.1 +/- 0.9 kg/m2). Before dex, glucose tolerance was similar in both groups (2-h plasma glucose concentration (PG): 5.5 +/- 0.2 [range: 3.2-7.0] vs 5.5 +/- 0.2 [3.7-7.4] mmol/l). Although insulin sensitivity (Si) was significantly lower in the relatives before dex, insulin sensitivity was reduced to a similar level during dex in both the relatives and control subjects (0.30 +/- 0.04 vs 0.34 +/- 0.04 10(-4) min(-1) per pmol/l, NS). During dex, the variation in the OGTT 2-h PG was greater in the relatives (8.5 +/- 0.7 [3.9-17.0] vs 7.5 +/- 0.3 [5.7-9.8] mmol/l, F-test p < 0.05) which, by inspection of the data, was caused by seven relatives with a higher PG than the maximal value seen in the control subjects (9.8 mmol/l). These "hyperglycaemic" relatives had diminished first phase insulin secretion (O1) both before and during dex compared with the "normal" relatives and the control subjects (pre-dex O1: 12.6 +/- 3.6 vs 26.4 +/- 4.2 and 24.6 +/- 3.6 (p < 0.05), post-dex O1: 22.2 +/- 6.6 vs 48.0 +/- 7.2 and 46.2 +/- 6.6 respectively (p < 0.05) pmol x l(-1) x min(-1) per mg/dl). However, Si was similar in "hyperglycaemic" and "normal" relatives before dex (0.65 +/- 0.10 vs 0.54 +/- 0.10 10(-4) x min(-1) per pmol/l) and suppressed similarly during dex (0.30 +/- 0.07 vs 0.30 +/- 0.06 10(-4) x min(-1) per pmol/l). Multiple regression analysis confirmed the unique importance of low pre-dex beta-cell function to subsequent development of high 2-h post-dex OGTT plasma glucose levels (R2 = 0.56). In conclusion, exogenous induced insulin resistance by dex will induce impaired or diabetic glucose tolerance in those genetic relatives of NIDDM patients who have impaired beta-cell function (retrospectively) prior to dex exposure. These subjects are therefore unable to enhance their beta-cell response in order to match the dex-induced insulin resistant state.

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  • The risk of diabetes was greater in subjects with abdominal adiposity or genetic predisposition and in those taking higher doses of glucocorticoids for longer periods.

    “The risk of DM was greater in subjects with abdominal adiposity or a genetic predisposition to DM and in those taking higher doses of GCs and for longer periods (, -).”

    From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [196]

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  1. [3]3. Kobberling J, Tillil H (1982) Empirical risk figures for firstdegree relatives of non-insulin dependent diabetics. In: Kobberling J, Tattersall R (eds) The genetics of diabetes mellitus. Academic Press, London New York, pp 202-209

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Authors
Alford, F., Beck-Nielsen, H., Ward, G. M., & Henriksen, J. E.
Affiliations
  • St Vincent's Hospital Melbourne (AU)
  • Odense University Hospital (DK)
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
1997-11-25
Volume
40
Issue
12
Pages
1439-1448
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s001250050847
OpenAlex
W1966238409
Cited by
115
References
48
Citations by year
2026: 1 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 6 · 2014: 9 · 2013: 7 · 2012: 6
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
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
dexamethasone, impaired glucose tolerance, insulin resistance, beta-cell function, first-phase insulin secretion, type 2 diabetes, first-degree relatives, genetic susceptibility to diabetes, insulin sensitivity
MeSH terms
Adult, Blood Glucose, C-Peptide, Dexamethasone, Diabetes Mellitus, Type 2, Female, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Cholesterol, HDL, Male, Risk Factors, Glucose Intolerance

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