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Codon 54 polymorphism of the fatty acid binding protein gene and insulin resistance in the Japanese population
Author(s) -
Ito K.,
Nakatani K.,
Fujii M.,
Katsuki A.,
Tsuchihashi K.,
Murata K.,
Goto H.,
Yano Y.,
Gabazza E. C.,
Sumida Y.,
Adachi Y.
Publication year - 1999
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1046/j.1464-5491.1999.00034.x
Subject(s) - insulin resistance , allele , biology , genetics , population , endocrinology , allele frequency , type 2 diabetes , medicine , restriction fragment length polymorphism , heterozygote advantage , insulin , gene , genotype , diabetes mellitus , environmental health
Summary Aim To determine the relationship of the polymorphism at codon 54 of the intestinal fatty acid binding protein gene (FABP2) with insulin resistance and susceptibility to Type 2 diabetes mellitus (DM) in the Japanese population. Methods We evaluated the polymorphism by the polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) in 150 Type 2 DM patients and 147 healthy control subjects. The frequency of alleles encoding threonine (Thr54) and alanine (Ala54) at codon 54 of FABP2 in Type 2 DM patients was compared with that of healthy controls. Insulin sensitivity was assessed by the hyperinsulinaemic euglycaemic clamp in Type 2 DM patients with Ala54 homozygotes, Ala54/Thr54 heterozygotes and Thr54 homozygotes and by homeostasis model assessment (HOMA) in the nondiabetic group. Results The frequency of alleles encoding Ala54 and Thr54 was 0.59 and 0.41 in Type 2 DM patients, respectively, similar to that observed in nondiabetic controls (0.64 for Ala54 and 0.36 for Thr54). Insulin sensitivity was not significantly different between subjects with and without Thr54 allele either within the DM group or healthy controls. Conclusions The allele encoding threonine in the FABP2 does not predispose to Type 2 DM or insulin resistance in the Japanese population Diabet. Med. 16, 119–124 (1999)