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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 3 1016-1019
Copyright © 1998 by The Endocrine Society


Original Studies

Mutation/Polymorphism Scanning of Glucose-6-Phosphatase Gene Promoter in Noninsulin-Dependent Diabetes Mellitus Patients1

Issei Yoshiuchi, Ryosuke Shingu, Hiromu Nakajima, Tomoya Hamaguchi, Yukio Horikawa, Tomoyuki Yamasaki, Takanori Oue, Akira Ono, Jun-ichiro Miyagawa, Mitsuyoshi Namba, Toshiaki Hanafusa and Yuji Matsuzawa

Second Department of Internal Medicine, Osaka University Medical School, 2–2 Yamadaoka, Suita, Osaka 565, Japan

Address all correspondence and requests for reprints to: Hiromu Nakajima, M.D., Ph.D., Second Department of Internal Medicine, Osaka University Medical School, 2–2 Yamadaoka, Suita, Osaka 565, Japan. E-mail: hinakaji{at}imed2.med.osaka-u.ac.jp

Glucose-6-phosphatase (G6Pase) catalyzes the rate-limiting step of gluconeogenesis, and hepatic G6Pase activity is increased in diabetes. We have cloned and analyzed the human G6Pase gene promoter region and identified putative regulatory sequences for insulin, cAMP, glucocorticoid, and hepatocyte nuclear factors. The promoter region of the G6Pase gene was analyzed in 154 noninsulin-dependent diabetes mellitus patients and 90 control subjects by PCR-single strand conformation polymorphism and direct sequencing methods. Polymorphisms were not found in any subjects. The results suggested that in noninsulin-dependent diabetic patients, the major cause of the hepatic glucose overproduction was not attributed to dysregulation of the G6Pase gene due to mutation/polymorphism of its promoter region.







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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
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Copyright © 1998 by The Endocrine Society