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J Biol Chem, Vol. 274, Issue 36, 25386-25392, September 3, 1999
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From the The NADH shuttle system is composed of the
glycerol phosphate and malate-aspartate shuttles. We generated mice
that lack mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH), a
rate-limiting enzyme of the glycerol phosphate shuttle. Application of
aminooxyacetate, an inhibitor of the malate-aspartate shuttle, to
mGPDH-deficient islets demonstrated that the NADH shuttle system was
essential for coupling glycolysis with activation of mitochondrial ATP
generation to trigger glucose-induced insulin secretion.
The present study revealed that blocking the NADH shuttle system
severely suppressed closure of the ATP-sensitive potassium (KATP) channel and depolarization of the plasma
membrane in response to glucose in Department of Metabolic Diseases and
Department of Physiology, Graduate School of Medicine,
University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan,
§ Department of Physiology, Hirosaki University School of
Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan, and ¶ Department
of Morphogenesis, Institute of Molecular Embryology and Genetics,
Kumamoto University School of Medicine, 4-24-1 Kuhonji, Kumamoto 862, Japan
cells, although properties of
the KATP channel on the excised cell membrane were
unaffected. In mGPDH-deficient islets treated with aminooxyacetate,
Ca2+ influx through the plasma membrane induced by a
depolarizing concentration of KCl in the presence of the
KATP channel opener diazoxide restored insulin secretion.
However, the level of the secretion was only ~40% of wild-type
controls. Thus, glucose metabolism through the NADH shuttle system
leading to efficient ATP generation is pivotal to activation of both
the KATP channel-dependent pathway and steps
distal to an elevation of cytosolic Ca2+ concentration in
glucose-induced insulin secretion.
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