Polymorphisms of the insulin gene among Japanese subjects

N. Oda; A. Nakai; K. Fujiwara; S. Imamura; T. Fujita; M. Hamagishi; T. Kato; T. Kobayashi; Y. Himeno; K. Yamamoto; M. Makino; H. Kakizawa; Y. Sawai; M. Itoh; A. Nagasaka

doi:10.1053/meta.2001.23283

Polymorphisms of the insulin gene among Japanese subjects

N. Oda, A. Nakai, K. Fujiwara, S. Imamura, T. Fujita, M. Hamagishi, T. Kato, T. Kobayashi, Y. Himeno, K. Yamamoto, M. Makino, H. Kakizawa, Y. Sawai, M. Itoh, A. Nagasaka

Internal Medicine

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). We identified 6 mutations and all were found at a low frequency (1% to 4%). Three mutations were new. These included a C-to-G substitution in the promoter region, a G-to-A substitution in codon-2 resulting in an Ala-to-Thr replacement in amino acid -2 of the signal peptide, and a G-to-A substitution in intron 2. We have no evidence that any of the mutations that we found are the cause of diabetes. Thus, mutations in the insulin gene do not appear to be an important genetic factor contributing to the development of diabetes in this population.

Original language	English
Pages (from-to)	631-634
Number of pages	4
Journal	Metabolism: Clinical and Experimental
Volume	50
Issue number	6
DOIs	https://doi.org/10.1053/meta.2001.23283
Publication status	Published - 2001

All Science Journal Classification (ASJC) codes

Endocrinology, Diabetes and Metabolism
Endocrinology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1053/meta.2001.23283

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abstract = "We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). We identified 6 mutations and all were found at a low frequency (1% to 4%). Three mutations were new. These included a C-to-G substitution in the promoter region, a G-to-A substitution in codon-2 resulting in an Ala-to-Thr replacement in amino acid -2 of the signal peptide, and a G-to-A substitution in intron 2. We have no evidence that any of the mutations that we found are the cause of diabetes. Thus, mutations in the insulin gene do not appear to be an important genetic factor contributing to the development of diabetes in this population.",

author = "N. Oda and A. Nakai and K. Fujiwara and S. Imamura and T. Fujita and M. Hamagishi and T. Kato and T. Kobayashi and Y. Himeno and K. Yamamoto and M. Makino and H. Kakizawa and Y. Sawai and M. Itoh and A. Nagasaka",

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T1 - Polymorphisms of the insulin gene among Japanese subjects

AU - Oda, N.

AU - Nakai, A.

AU - Fujiwara, K.

AU - Imamura, S.

AU - Fujita, T.

AU - Hamagishi, M.

AU - Kato, T.

AU - Kobayashi, T.

AU - Himeno, Y.

AU - Yamamoto, K.

AU - Makino, M.

AU - Kakizawa, H.

AU - Sawai, Y.

AU - Itoh, M.

AU - Nagasaka, A.

PY - 2001

Y1 - 2001

N2 - We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). We identified 6 mutations and all were found at a low frequency (1% to 4%). Three mutations were new. These included a C-to-G substitution in the promoter region, a G-to-A substitution in codon-2 resulting in an Ala-to-Thr replacement in amino acid -2 of the signal peptide, and a G-to-A substitution in intron 2. We have no evidence that any of the mutations that we found are the cause of diabetes. Thus, mutations in the insulin gene do not appear to be an important genetic factor contributing to the development of diabetes in this population.

AB - We have sequenced the insulin gene in 72 unrelated Japanese subjects (52 with type 2 diabetes mellitus and 20 with normal glucose tolerance). We identified 6 mutations and all were found at a low frequency (1% to 4%). Three mutations were new. These included a C-to-G substitution in the promoter region, a G-to-A substitution in codon-2 resulting in an Ala-to-Thr replacement in amino acid -2 of the signal peptide, and a G-to-A substitution in intron 2. We have no evidence that any of the mutations that we found are the cause of diabetes. Thus, mutations in the insulin gene do not appear to be an important genetic factor contributing to the development of diabetes in this population.

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JO - Metabolism: Clinical and Experimental

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Polymorphisms of the insulin gene among Japanese subjects

Abstract

All Science Journal Classification (ASJC) codes

UN SDGs

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