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Cited by 83Genetic Associations and EpidemiologyAdipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and Lipoproteins

Association of obesity, but not diabetes or hypertension, with glucocorticoid receptor N363S variant

Lin, Ruby C.Y., Wang, Xing Li, Dalziel, Bronwen, Caterson, Ian D., Morris, Brian J.·2003·Obesity Research
DOI 10.1038/oby.2003.111
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Abstract

OBJECTIVE: To determine whether the N363S variant in the glucocorticoid receptor (encoded by nuclear receptor subfamily 3, group C, member 1: NR3C1) is associated with obesity, type 2 diabetes, or hypertension. RESEARCH METHODS AND PROCEDURES: This was a cross-sectional case-control study involving 951 Anglo-Celtic/Northern European subjects from Sydney. This study consisted of the following: 1) an obesity clinic group, most of whom had "morbid obesity" (mean BMI for group = 43 +/- 8 kg/m(2); n = 152); 2) a type 2 diabetes clinic group (n = 356); 3) patients with essential hypertension who had a strong family history (n = 141); and 4) normal healthy controls (n = 302). N363S genotype, BMI, and a range of other parameters relevant to each group were measured. RESULTS: Compared with the frequency of 0.04 in nonobese healthy subjects, the S363 allele was significantly higher in obesity clinic patients (0.17; p = 5.6 x 10(-8)), subjects with diabetes who were also obese (0.09; p = 0.0045), subjects with hypertension who were also overweight (0.08; p = 0.0016), and overweight healthy subjects (0.12; p = 0.0004). DISCUSSION: The NR3C1 N363S variant is associated with obesity and overweight in a range of patient settings but is not associated with hypertension or type 2 diabetes.

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  • Interindividual sensitivity to glucocorticoids is influenced, in part, by polymorphisms in the glucocorticoid receptor gene, which have been associated with altered receptor function and differential metabolic responses to cortisol.

    “This variability is influenced, in part, by polymorphisms in the glucocorticoid receptor gene, which have been associated with altered receptor function and differential metabolic responses to cortisol (102-108).”

    From Measuring cortisol in Cushing syndrome: diagnosis, monitoring, and cortisol circadian rhythm improvement. (2026) · cites this paper as [103]

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Authors
Lin, R. C. Y., Wang, X. L., Dalziel, B., Caterson, I. D., & Morris, B. J.
Affiliations
  • The University of Sydney (AU)
  • Texas Biomedical Research Institute (US)
Corresponding author
Morris, Brian J.
ORCID
Venue
Obesity Research
Publisher
Wiley
Published
2003-06
Volume
11
Issue
6
Pages
802-808
ISSN
  • 1071-7323 (ISSN-L)
  • 1550-8528
DOI
10.1038/oby.2003.111
OpenAlex
W2060018442
Cited by
83
References
2
Citations by year
2026: 2 · 2025: 1 · 2024: 4 · 2021: 4 · 2020: 2 · 2019: 5 · 2018: 1 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 5
FWCI
3.20
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3385 d)
Locations
  • Obesity Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Health and Medical Research Council
  • National Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
glucocorticoid receptor, NR3C1, N363S polymorphism, obesity, type 2 diabetes, essential hypertension, overweight, genetic association, morbid obesity, body mass index
MeSH terms
Adult, Aged, Alleles, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Female, Genotype, Humans, Hypertension, Male, Middle Aged, Obesity, Receptors, Glucocorticoid, Sex Characteristics, Genetic Variation, Cohort Studies, Body Mass Index, Case-Control Studies

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