RGD Reference Report - Exaggerated adrenarche and altered cortisol metabolism in Type 1 diabetic children. - Rat Genome Database

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Exaggerated adrenarche and altered cortisol metabolism in Type 1 diabetic children.

Authors: Remer, T  Maser-Gluth, C  Boye, KR  Hartmann, MF  Heinze, E  Wudy, SA 
Citation: Remer T, etal., Steroids. 2006 Jul;71(7):591-8. Epub 2006 Apr 17.
RGD ID: 2308923
Pubmed: PMID:16616286   (View Abstract at PubMed)
DOI: DOI:10.1016/j.steroids.2006.02.005   (Journal Full-text)

Reported literature data strongly suggest that steroid metabolism is dysregulated in Type 1 diabetes mellitus. The aim of this study was to non-invasively examine the cortisol metabolism in children with Type 1 diabetes mellitus (T1DM) in detail and to test the hypothesis that adrenarche is affected under conventional intensive insulin therapy. In 24-h urine samples of 109 patients aged 4-18 years with T1DM of more than 1 year, steroids were profiled using gas chromatography-mass spectrometry. Additionally, urinary free cortisol (UFF) and cortisone (UFE) were quantified by RIA after extraction and chromatographic purification. Data on urinary steroids from 400 healthy controls served as reference values. Enzyme activities were assessed by established steroid metabolite ratios, e.g. 5alpha-reductase and 11beta-hydroxysteroid dehydrogenase Type 2 (11beta-HSD2) by 5alpha-tetrahydrocortisol/tetrahydrocortisol and UFE/UFF, respectively. Urinary markers of adrenarche, especially dehydroepiandrosterone and its direct metabolites were elevated in patients, as were urinary 6beta-hydroxycortisol, UFE, and 11beta-HSD2 activity. However, overall cortisol secretion, as reflected by the sum of major urinary cortisol metabolites, was mostly normal and activity of 5alpha-reductase clearly reduced. Our study provides evidence for an exaggerated adrenarche in T1DM children, which may help to understand reported sequelae in female patients like hyperandrogenic symptoms. The findings also suggest a reduced cortisol inactivation via 5alpha-reductase that is not compensated by a fall in cortisol secretion. Whether the elevated urinary 6beta-hydroxycortisol and cortisone excretion, observed in the patients, are also present in other forms of hypercortisolism and may thus serve as non-invasive clinical stress markers deserves further study.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
HSD11B2Humantype 1 diabetes mellitus  IEP  RGD 
Hsd11b2Rattype 1 diabetes mellitus  ISOHSD11B2 (Homo sapiens) RGD 
Hsd11b2Mousetype 1 diabetes mellitus  ISOHSD11B2 (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Hsd11b2  (hydroxysteroid 11-beta dehydrogenase 2)

Genes (Mus musculus)
Hsd11b2  (hydroxysteroid 11-beta dehydrogenase 2)

Genes (Homo sapiens)
HSD11B2  (hydroxysteroid 11-beta dehydrogenase 2)


Additional Information