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Science 12 February 1999:
Vol. 283. no. 5404, pp. 981 - 985
DOI: 10.1126/science.283.5404.981
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Reports

Role of NADH Shuttle System in Glucose-Induced Activation of Mitochondrial Metabolism and Insulin Secretion

Kazuhiro Eto, 1 Yoshiharu Tsubamoto, 1 Yasuo Terauchi, 1 Takuya Sugiyama, 1 Takuya Kishimoto, 2 Noriko Takahashi, 1 Naoko Yamauchi, 3 Naoto Kubota, 1 Shigeo Murayama, 4 Toru Aizawa, 5 Yasuo Akanuma, 6 Shinichi Aizawa, 7 Haruo Kasai, 2 Yoshio Yazaki, 1 Takashi Kadowaki 1*

Glucose metabolism in glycolysis and in mitochondria is pivotal to glucose-induced insulin secretion from pancreatic beta  cells. One or more factors derived from glycolysis other than pyruvate appear to be required for the generation of mitochondrial signals that lead to insulin secretion. The electrons of the glycolysis-derived reduced form of nicotinamide adenine dinucleotide (NADH) are transferred to mitochondria through the NADH shuttle system. By abolishing the NADH shuttle function, glucose-induced increases in NADH autofluorescence, mitochondrial membrane potential, and adenosine triphosphate content were reduced and glucose-induced insulin secretion was abrogated. The NADH shuttle evidently couples glycolysis with activation of mitochondrial energy metabolism to trigger insulin secretion.

1 Department of Internal Medicine;
2 Department of Physiology;
3 Department of Pathology;
4 Department of Neurology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.
5 Department of Geriatrics, Endocrinology and Metabolism, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390, Japan.
6 Institute for Diabetes Care and Research, Asahi Life Foundation, 1-6-1 Marunouchi, Chiyoda-ku, Tokyo 100, Japan.
7 Department of Morphogenesis, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, 4-24-1 Kuhonji, Kumamoto 862, Japan.
*   To whom correspondence should be addressed. E-mail: kadowaki-3im{at}h.u-tokyo.ac.jp

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