April 1, 1997Diabetes
Genetic Studies of the Sulfonylurea Receptor Gene Locus in NIDDM and in Morbid Obesity Among French Caucasians
Key result
SUR gene exon 22 T-allele linked to NIDDM and ~271% higher morbid obesity risk.
- OR 3.71
- P=0.017
Why the study?
Obesity and NIDDM share metabolic abnormalities suggesting common susceptibility genes, making the SUR gene a plausible candidate for beta-cell defects contributing to hyperglycemia and weight gain.
Population
French Caucasian families with NIDDM and two independent sets of morbidly obese families
Comparison
Patients with NIDDM and morbid obesity vs control subjects
Design
Association and linkage case-control studies
Authors
Discussion
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Overview
SUR variants associated with NIDDM and obesity risk; leaves open causal contribution and warrants larger replication before clinical consideration.
Study Design
Type
Case-Control
Structured PICO
P
Population
French Caucasian families with NIDDM and morbid obesity, along with control subjects, evaluated for SUR gene variants.
C
Comparator
Control subjects
O
Outcome
Association and linkage of SUR gene variants (exon 22 T-allele, intron 24 variant, microsatellite marker D11S419) with NIDDM and morbid obesitysurrogate
Main Result
Odds Ratio: 3.71
Absolute Event Rate: 7.8% vs 1.8%
p-value: p=0.017
The sulfonylurea receptor (SUR) gene locus may contribute to genetic susceptibility to NIDDM and morbid obesity in French Caucasians.
Cite This Study
Hani et al. (1997) conducted a case-control in NIDDM and morbid obesity. Exon 22 T-allele at codon 761 of the SUR gene vs. Control subjects was evaluated on Morbid obesity (OR 3.71, p=0.017). The exon 22 T-allele of the SUR gene was significantly associated with morbid obesity (OR 3.71, P=0.017) and NIDDM (OR 2.20, P=0.04) in French Caucasians.