Mutation in Bombesin Receptor Subtype-3 Gene is not a Major Cause of Obesity in the Japanese

K. Hotta; Y. Matsukawa; M. Nishida; K. Kotani; M. Takahashi; H. Kuriyama; T. Nakamura; K. Wada; S. Yamashita; T. Funahashi; Y. Matsuzawa

doi:10.1055/s-2007-978582

Hormone and Metabolic Research, Table of Contents

Horm Metab Res 2000; 32(1): 33-34
DOI: 10.1055/s-2007-978582

Originals Clinical

Mutation in Bombesin Receptor Subtype-3 Gene is not a Major Cause of Obesity in the Japanese

K. Hotta¹ , Y. Matsukawa¹ , M. Nishida¹ , K. Kotani¹ , M. Takahashi¹ , H. Kuriyama¹ , T. Nakamura¹ , K. Wada² , S. Yamashita¹ , T. Funahashi¹ , Y. Matsuzawa¹

¹Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
²Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan

Abstract

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Bombesin receptor subtype-3 (BRS-3) is one of the candidate genes of obesity. The mice lacking BRS-3 have been shown to develop mild obesity. These mice also showed hypertension and impaired glucose metabolism, supporting these mice as a good model for human obesity. We screened 104 Japanese obese men (BMI > 26.4, 26.5-44.1) to investigate whether there is any genetic defect in BRS-3 gene. The DNA fragments containing each exon of BRS-3 gene were amplified by polymerase chain reaction (PCR) and were directly sequenced. No mutation, nor polymorphism was found in the coding region of BRS3, suggesting that mutation of this gene is not a major cause of obesity in humans.

Key words

Bombesin Receptor Subtype-3 - Obesity - Japanese

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