The mouse obese (ob) gene has recently been isolated through the positional cloning technique and has been proved to result in the obese and NIDDM phenotype in mice when mutated (Nature 372:425–432, 1994). More recently, it has been demonstrated, by experiments with recombinant ob protein, that ob gene product can cause mice, including ob/ob mice, diet-induced obesity mice, and normal mice, to lower their food intake and body weight (Science 269:540–549, 1995). To investigate the genetic and/or environmental influences underlying the development of NIDDM associated with obesity, we isolated and partially sequenced the human obese (OB) gene. The human OB gene isolated in this study encoded 167 amino acids and its open reading frame was revealed to be divided into two parts with an intermediate intron of ∼2.4 kb. Using the single-strand conformation polymorphism (SSCP) technique, we screened Japanese and Asian Indian subjects for mutations in the protein coding regions of the OB gene. A total of 75 NIDDM patients with obesity (54 Japanese and 21 Asian Indians), 40 NIDDM patients without obesity (34 Japanese and 6 Asian Indians), and 34 Japanese patients with simple obesity showed no abnormal SSCP patterns in either component of the coding sequences. These results suggested that mutations in the coding regions of the OB gene are not likely to be commonly identifiable and that there would likely be a kind of obesity-associated NIDDM not caused by mutations of the OB gene.
Human Obese Gene: Molecular Screening in Japanese and Asian Indian NIDDM Patients Associated With Obesity
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Toshiharu Niki, Hiroyuki Mori, Yoshikazu Tamori, Miyako Kishimoto-Hashirmoto, Hirohisa Ueno, Satoshi Araki, Jiro Masugi, Nitin Sawant, Hemali R Majithia, Nadeem Rais, Mitsuru Hashiramoto, Hiroshi Taniguchi, Masato Kasuga; Human Obese Gene: Molecular Screening in Japanese and Asian Indian NIDDM Patients Associated With Obesity. Diabetes 1 May 1996; 45 (5): 675–678. https://doi.org/10.2337/diab.45.5.675
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