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Endocrinology Vol. 140, No. 10 4706-4712
Copyright © 1999 by The Endocrine Society

ARTICLES

An Insulinotropic Effect of Vitamin D Analog with Increasing Intracellular Ca2+ Concentration in Pancreatic ß-Cells through Nongenomic Signal Transduction1

Mariko Kajikawa, Hitoshi Ishida, Shimpei Fujimoto, Eri Mukai2, Masayoshi Nishimura, Jun Fujita, Yoshiyuki Tsuura, Yoshimasa Okamoto, Anthony W. Norman and Yutaka Seino

Department of Metabolism and Clinical Nutrition (M.K., S.F., E.M., M.N., J.F., Y.T., Y.O., Y.S.), Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan; Third Department of Internal Medicine (H.I.), Kyorin University School of Medicine, Mitaka, Tokyo 181-8611 Japan; and Department of Biochemistry (A.W.N.), University of California, Riverside, California 92521

Address all correspondence and requests for reprints to: Mariko Kajikawa M.D., Department of Metabolism & Clinical Nutrition, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: kajikawa{at}metab.kuhp.kyoto-u.ac.jp

The effect of 1{alpha},25-dihydroxylumisterol3 (1{alpha},25(OH)2lumisterol3) on insulin release from rat pancreatic ß-cells was measured to investigate the nongenomic action of vitamin D via the putative membrane vitamin D receptor (mVDR). 1{alpha},25(OH)2lumisterol3, a specific agonist of mVDR, dose-dependently augmented 16.7 mM glucose-induced insulin release from rat pancreatic islets and increased the intracellular Ca2+ concentration ([Ca2+]i), though not increasing Ca2+ efficacy in the exocytotic system. These effects were completely abolished by an antagonist of mVDR, 1ß,25-dihydroxyvitamin D3 (1ß,25(OH)2D3), or by a blocker of voltage-dependent Ca2+ channels, nitrendipine. Moreover, both [Ca2+]i elevation, caused by membrane depolarization, and sufficient intracellular glucose metabolism are required for the expression of these effects. 1{alpha},25(OH)2lumisterol3, therefore, has a rapid insulinotropic effect, through nongenomic signal transduction via mVDR, that would be dependent on the augmentation of Ca2+ influx through voltage-dependent Ca2+ channels on the plasma membrane, being also linked to metabolic signals derived from glucose in pancreatic ß-cells. However, further investigations will be needed to discuss physiologically the meaning of insulinotropic effects of vitamin D through mVDR.




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