Association of the T-G Polymorphism in Adiponectin (Exon 2) With Obesity and Insulin Sensitivity
Abstract
The adipocyte-derived hormone adiponectin seems to protect from insulin resistance, a key factor in the pathogenesis of type 2 diabetes. Genome-wide scans have mapped a susceptibility locus for type 2 diabetes and the metabolic syndrome to chromosome 3q27, where the adiponectin gene is located. A common silent T-G exchange in nucleotide 94 (exon 2) of the adiponectin gene has been associated with increased circulating adiponectin levels. Metabolic abnormalities associated with the G allele have not been reported. We therefore assessed whether this polymorphism alters insulin sensitivity and/or measures of obesity using the Tübingen Family Study database (prevalence of the G allele, 28%). In 371 nondiabetic individuals, we found a significantly greater BMI in GG + GT (25.5 ± 0.7 kg/m2) compared with TT (24.1 ± 0.3 kg/m2; P = 0.02). Insulin sensitivity (determined by euglycemic clamp, n = 209) was significantly lower in GG + GT (0.089 ± 0.007 units) compared with TT (0.112 ± 0.005 units; P = 0.02). This difference disappeared completely on adjustment for BMI. Because our population contains a relatively high proportion of first-degree relatives of patients with type 2 diabetes, we stratified by family history (FHD). Much to our surprise, the genotype differences in BMI and insulin sensitivity in the whole population were attributable entirely to differences in the subgroup without FHD, whereas in the subgroup with FHD, the G allele had absolutely no effect. Moreover, individuals without FHD had a significantly lower BMI than individuals with FHD (25.2 ± 0.4 vs. 26.2 ± 0.5 kg/m2; P = 0.01), which was not the case for the GG + GT subgroup without FHD (27.0 ± 0.9 kg/m2; NS). This suggests that in individuals without familial predisposition for type 2 diabetes, the adiponectin polymorphism may mildly increase the obesity risk (and secondarily insulin resistance). In contrast, in individuals who are already burdened by other genetic factors, this small effect may be very hard to detect.
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Known genetic mutations associated with insulin resistance are rare in healthy subjects across populations.
“Examination of groups of healthy subjects in a number of different populations has shown that known genetic mutations associated with insulin resistance are rare [20, 39, 40, 41, 42, 43, 44].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [44]
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- Authors
- Stumvoll, M., Tschritter, O., Fritsche, A., Staiger, H., Renn, W., Weisser, M., Machicao, F., & Häring, H.
- Affiliations
- Medizinische Klinik, Abteilung für Endokrinologie, Stoffwechsel und Pathobiochemie, Eberhard-Karls-Universität, Tübingen, Germany
- University of Tübingen (DE)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-01-01
- Volume
- 51
- Issue
- 1
- Pages
- 37-41
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2106550052
- Cited by
- 371
- References
- 16
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 9 · 2020: 6 · 2019: 8 · 2018: 8 · 2017: 11 · 2016: 14 · 2015: 14 · 2014: 18 · 2013: 17 · 2012: 14
- FWCI
- 24.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- adiponectin, exon 2, obesity, insulin sensitivity, insulin resistance, type 2 diabetes risk, family history of diabetes, body mass index, chromosome 3q27, genetic association
- MeSH terms
- Adult, Alleles, Blood Glucose, Body Composition, Chromosome Mapping, Chromosomes, Human, Pair 3, Diabetes Mellitus, Type 2, Exons, Female, Glucose Tolerance Test, Humans, Insulin, Male, Obesity, Polymorphism, Genetic, Proteins, Reference Values, Body Mass Index, Adipocytes, Intercellular Signaling Peptides and Proteins, Adiponectin
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