Genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributed to NIDDM development, with the APOA1/C3/A4 locus accounting for approximately 8% of the risk difference in overweight individuals.
Case-Control
The frequencies of restriction-fragment-length polymorphism (RFLP) alleles as well as RFLP haplotypes at six genetic loci responsible for carbohydrate and lipid metabolism insulin/insulin-like growth factor II complex, insulin receptor (INSR), HepG2/erythrocyte-type glucose transporter, apolipoprotein A-II, apolipoprotein B (APOB), and the apolipoprotein A-I/C-III/A-IV cluster (APOA1/C3/A4) were compared between nondiabetic and diabetic Chinese Americans. The disease-association data suggest that genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributes to the development of non-insulin-dependent diabetes mellitus (NIDDM). The analysis of the INSR locus revealed "protective" haplotypes, and it may be possible to use two of the INSR haplotypes as genetic markers to identify individuals having a very low probability of developing NIDDM regardless of the presence of other genes conferring susceptibility to this disorder. The APOB and APOA1/C3/A4 loci appear to contribute to the development of NIDDM in individuals who are of lean/normal weight and overweight, respectively. The APOA1/C3/A4 locus may account for approximately 8% of the difference between baseline and total possible risk of NIDDM in overweight individuals.
Xiang et al. (Sun,) conducted a case-control in Non-insulin-dependent diabetes mellitus (NIDDM). Genetic variation at INSR, APOB, and APOA1/C3/A4 loci vs. Nondiabetic controls was evaluated on Development of NIDDM. Genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributed to NIDDM development, with the APOA1/C3/A4 locus accounting for approximately 8% of the risk difference in overweight individuals.
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