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509 results on '"Kakei, Masafumi"'

2. ELKS/Voltage-Dependent Ca2+ Channel-β Subunit Module Regulates Polarized Ca2+ Influx in Pancreatic β Cells

Author

Ohara-Imaizumi, Mica, Aoyagi, Kyota, Yamauchi, Hajime, Yoshida, Masashi, Mori, Masayuki X., Hida, Yamato, Tran, Ha Nam, Ohkura, Masamichi, Abe, Manabu, Akimoto, Yoshihiro, Nakamichi, Yoko, Nishiwaki, Chiyono, Kawakami, Hayato, Hara, Kazuo, Sakimura, Kenji, Nagamatsu, Shinya, Mori, Yasuo, Nakai, Junichi, Kakei, Masafumi, and Ohtsuka, Toshihisa

Published
2019
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3. Serotonin regulates glucose-stimulated insulin secretion from pancreatic β cells during pregnancy

Author

Ohara-Imaizumi, Mica, Kim, Hail, Yoshida, Masashi, Fujiwara, Tomonori, Aoyagi, Kyota, Toyofuku, Yukiko, Nakamichi, Yoko, Nishiwaki, Chiyono, Okamura, Tadashi, Uchida, Toyoyoshi, Fujitani, Yoshio, Akagawa, Kimio, Kakei, Masafumi, Watada, Hirotaka, German, Michael S, and Nagamatsu, Shinya

Subjects
Diabetes, Underpinning research, 1.1 Normal biological development and functioning, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Animals, Female, Glucose, Immunoblotting, Immunohistochemistry, Insulin, Insulin Secretion, Insulin-Secreting Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Fluorescence, Pregnancy, Receptors, Serotonin, 5-HT3, Serotonin, Signal Transduction
Abstract

In preparation for the metabolic demands of pregnancy, β cells in the maternal pancreatic islets increase both in number and in glucose-stimulated insulin secretion (GSIS) per cell. Mechanisms have been proposed for the increased β cell mass, but not for the increased GSIS. Because serotonin production increases dramatically during pregnancy, we tested whether flux through the ionotropic 5-HT3 receptor (Htr3) affects GSIS during pregnancy. Pregnant Htr3a(-/-) mice exhibited impaired glucose tolerance despite normally increased β cell mass, and their islets lacked the increase in GSIS seen in islets from pregnant wild-type mice. Electrophysiological studies showed that activation of Htr3 decreased the resting membrane potential in β cells, which increased Ca(2+) uptake and insulin exocytosis in response to glucose. Thus, our data indicate that serotonin, acting in a paracrine/autocrine manner through Htr3, lowers the β cell threshold for glucose and plays an essential role in the increased GSIS of pregnancy.

Published
2013

4. Effect of an intensified multifactorial intervention on cardiovascular outcomes and mortality in type 2 diabetes (J-DOIT3): an open-label, randomised controlled trial

Author

Haneda, Masakazu, Iwashima, Yasunori, Suda, Toshihiro, Tamasawa, Naoki, Daimon, Makoto, Satoh, Jo, Takebe, Noriko, Ishigaki, Yasushi, Watanabe, Tsuyoshi, Satoh, Hiroaki, Kasai, Kikuo, Aso, Yoshimasa, Ishibashi, Shun, Katayama, Shigehiro, Ishikawa, San-e, Kakei, Masafumi, Namai, Kazuyuki, Hashimoto, Naotake, Suzuki, Yoshifumi, Onishi, Shunichiro, Yokote, Koutaro, Matsuda, Masafumi, Masuzawa, Masahiro, Hayashi, Yoichi, Saito, Satoshi, Ogihara, Norikazu, Ishihara, Hisamitsu, Tajima, Naoko, Utsunomiya, Kazunori, Shimada, Akira, Itoh, Hiroshi, Kawamori, Ryuzo, Watada, Hirotaka, Hayashi, Michio, Mori, Yasumichi, Shiba, Teruo, Isogawa, Akihiro, Sakura, Hiroshi, Odawara, Masato, Tobe, Kazuyuki, Tsukamoto, Kazuhisa, Yamauchi, Toshimasa, Teramoto, Tamio, Hirata, Yukio, Uchimura, Isao, Ogawa, Yoshihiro, Yoshino, Gen, Hirose, Takahisa, Kajio, Hiroshi, Atsumi, Yoshihito, Oikawa, Yoichi, Araki, Atsushi, Ueki, Akio, Ohno, Atsushi, Kitaoka, Masafumi, Fujita, Yoshikuni, Moriya, Tatsumi, Tojo, Taiki, Shichiri, Masayoshi, Suzuki, Daisuke, Toyoda, Masao, Hamano, Kumiko, Komi, Rieko, Terauchi, Yasuo, Kuzuya, Nobuaki, Yamada, Masayo, Takamura, Toshinari, Imura, Mitsuo, Tanaka, Hiroshi, Hayashi, Masayuki, Kato, Yasuhisa, Itoh, Mitsuyasu, Suzuki, Atsushi, Nakayama, Mikihiro, Sano, Takahisa, Nakashima, Eitaro, Sumida, Yasuhiro, Yano, Yutaka, Tanaka, Tsuyoshi, Murata, Kazuya, Kashiwagi, Atsunori, Maegawa, Hiroshi, Kono, Shigeo, Inagaki, Nobuya, Kosugi, Keisuke, Yasuda, Tetsuyuki, Yoshimasa, Yasunao, Kishimoto, Ichiro, Sato, Toshihiko, Hosoi, Masayuki, Yamasaki, Tomoyuki, Matsuhisa, Munehide, Shimomura, Iichiro, Taniguchi, Ataru, Kuroe, Akira, Kurose, Takeshi, Ohara, Takeshi, Sakaguchi, Kazuhiko, Namba, Mitsuyoshi, Kaku, Kohei, Fujiwara, Masazumi, Shimizu, Ikki, Ono, Keizo, Ebisui, Osamu, Tanizawa, Yukio, Okada, Yosuke, Natori, Shoichi, Kodera, Takehiko, Sato, Naoichi, Ide, Makoto, Yamada, Kentaro, Umeda, Fumio, Eto, Tomoaki, Mimura, Kazuo, Hiramatsu, Shinsuke, Inoue, Tomoaki, Takei, Ryoko, Ogo, Atsushi, Eguchi, Katsumi, Kawasaki, Eiji, Koide, Yuji, Araki, Eiichi, Jinnouchi, Hideaki, Yamamoto, Hiroaki, Motoyoshi, Mitsutaka, Hiyoshi, Toru, Tanaka, Yasushi, Momoki, Tadahisa, Sato, Koichiro, Yoneyama, Akihiko, Ito, Kenichi, Sobajima, Hiroshi, Ikegami, Hiroshi, Ikeda, Masaki, Ikeda, Hiroki, Takahashi, Kenji, Makino, Hirofumi, Ueda, Yasuo, Nakazato, Masamitsu, Ueki, Kohjiro, Sasako, Takayoshi, Okazaki, Yukiko, Kato, Masayuki, Okahata, Sumie, Katsuyama, Hisayuki, Haraguchi, Mikiko, Morita, Ai, Ohashi, Ken, Hara, Kazuo, Morise, Atsushi, Izumi, Kazuo, Ishizuka, Naoki, Ohashi, Yasuo, Noda, Mitsuhiko, and Kadowaki, Takashi

Published
2017
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14. Cerebral oxygenation changes in response to post-hemodialysis standing

Author

Imai, Sojiro, primary, Ookawara, Susumu, additional, Ito, Kiyonori, additional, Hattori, Takashi, additional, Fueki, Mariko, additional, Iguchi, Miho, additional, Kiryu, Satoshi, additional, Sanayama, Hidenori, additional, Kakei, Masafumi, additional, Tabei, Kaoru, additional, and Morishita, Yoshiyuki, additional

Published
2022
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26. Class IA Phosphatidylinositol 3-Kinase in Pancreatic β Cells Controls Insulin Secretion by Multiple Mechanisms

Author

Kaneko, Kazuma, Ueki, Kohjiro, Takahashi, Noriko, Hashimoto, Shinji, Okamoto, Masayuki, Awazawa, Motoharu, Okazaki, Yukiko, Ohsugi, Mitsuru, Inabe, Kazunori, Umehara, Toshihiro, Yoshida, Masashi, Kakei, Masafumi, Kitamura, Tadahiro, Luo, Ji, Kulkarni, Rohit N., Kahn, C. Ronald, Kasai, Haruo, Cantley, Lewis C., and Kadowaki, Takashi

Published
2010
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30. Muscle mass evaluation using psoas muscle mass index by computed tomography imaging in hemodialysis patients

Author

Ito, Kiyonori, primary, Ookawara, Susumu, additional, Imai, Sojiro, additional, Kakuda, Hideo, additional, Bandai, Yusaku, additional, Fueki, Mariko, additional, Yasuda, Masatoshi, additional, Kamimura, Tatsuya, additional, Kiryu, Satoshi, additional, Wada, Noriko, additional, Hamashima, Yuri, additional, Shindo, Mitsutoshi, additional, Kobayashi, Tadanao, additional, Sanayama, Hidenori, additional, Kaku, Yoshio, additional, Tanno, Keisuke, additional, Ohnishi, Yasushi, additional, Iino, Noriaki, additional, Dezaki, Katsuya, additional, Kakei, Masafumi, additional, Tabei, Kaoru, additional, and Morishita, Yoshiyuki, additional

Published
2021
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31. Vital signs, QT prolongation, and newly diagnosed cardiovascular disease during severe hypoglycemia in type 1 and type 2 diabetic patients

Author

Tsujimoto, Tetsuro, Yamamoto-Honda, Ritsuko, Kajio, Hiroshi, Kishimoto, Miyako, Noto, Hiroshi, Hachiya, Remi, Kimura, Akio, Kakei, Masafumi, and Noda, Mitsuhiko

Subjects
Diabetes -- Risk factors -- Diagnosis -- Care and treatment, Cardiovascular diseases -- Risk factors -- Diagnosis -- Care and treatment, Hypoglycemia -- Risk factors -- Diagnosis -- Care and treatment, Health
Abstract

OBJECTIVE To assess vital signs, QT intervals, and newly diagnosed cardiovascular disease during severe hypoglycemia in diabetic patients. RESEARCH DESIGN AND METHODS From January 2006 to March 2012, we conducted [...]

Published
2014
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38. Regulation of [K.sub.ATP] channels by [P.sub.2Y] purinoceptors coupled to PI[P.sub.2] metabolism in guinea pig ventricular cells

Author

Oketani, Naoya, Kakei, Masafumi, Ichinari, Kotaro, Okamura, Midori, Miyamura, Akihiro, Nakazaki, Mitsuhiro, Ito, Seiki, and Tei, Chuwa

Subjects
Physiology -- Research, Potassium channels -- Research, Heart ventricles -- Research, Biological sciences
Abstract

Regulation of [K.sub.ATP] channels by [P.sub.2Y] purinoceptors coupled to PI[P.sub.2] metabolism in guinea pig ventricular cells. Am J Physiol Heart Circ Physiol 282: H757-H765, 2002. First published October 11, 2001; 10.1152/ ajpheart.00246.2001.--We used patch-clamp techniques to elucidate the regulatory mechanisms of ATP-sensitive [K.sup.+] ([K.sub.ATP]) channels by stimulation of [P.sub.2] purinoceptors in guinea pig ventricular myocytes. Extracellular ATP at 0.1 mM transiently inhibited by 90.5 [+ or -] 5.0% the whole cell [K.sub.ATP] channel current evoked by a reduction in intracellular ATP concentration to 0.5 mM and exposure to 30 [micro]M pinacidil. ADP and AMP (both 1 mM) also decreased the current by 42.8 [+ or -] 9.3% and 9.4 [+ or -] 4.8%, respectively, but adenosine did not, even at 10 mM. ATP-induced channel inhibition was hardly observed in the presence of 0.2 mM suramin, 0.2 mM guanosine 5'-O-(2-thiodiphosphate), or 0.1 mM compound 48/80, whereas it was not influenced by the presence of 0.1 [micro]M staurosporine or 10 mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid in the pipette. In the presence of 10 [micro]M wortmannin or the absence of ATP in the cytosol, the ATP-induced channel inhibition was irreversible. Phosphatidylinositol 4,5-bisphosphate (PI[P.sub.2]) at 0.1 mM in the outside-out patch pipette prevented ATP-induced channel inhibition. The half-maximal internal ATP concentrations for inhibition of channel activity determined in inside-out membrane patches were 13.8 [micro]M in the presence and 1.12 mM in the absence of 0.1 mM ATP at the external side. It is concluded that activity of [K.sub.ATP] channels is modulated by extracellular ATP by a mechanism involving [P.sub.2Y] purinoceptors coupled to GTP-binding proteins associated with reduction of the sarcolemmal PI[P.sub.2] concentration via stimulation of phospholipase C. phosphatidylinositol 4,5-bisphosphate, extracellular adenosine 5'-triphosphate; phosphatidylinositol turnover; phospholipase C

Published
2002

41. A novel mechanism of imeglimin‐mediated insulin secretion via the cADPR‐TRP channel pathway.

Author

Funazaki, Shunsuke, Yoshida, Masashi, Yamada, Hodaka, Kakei, Masafumi, Kawakami, Masanobu, Nagashima, Shuichi, Hara, Kazuo, and Dezaki, Katsuya

Subjects
INSULIN, SECRETION, NAD (Coenzyme), BLOOD sugar, HYPOGLYCEMIC agents, TYPE 2 diabetes
Abstract

Aims/Introduction: Imeglimin is a novel oral hypoglycemic agent that improves blood glucose levels through multiple mechanisms of action including the enhancement of glucose‐stimulated insulin secretion (GSIS), however, the details of this mechanism have not been clarified. In the process of GSIS, activation of the transient receptor potential melastatin 2 (TRPM2) channel, a type of non‐selective cation channel (NSCCs) in β‐cells, promotes plasma membrane depolarization. The present study aimed to examine whether imeglimin potentiates GSIS via the TRPM2 channel in β‐cells. Materials and Methods: Pancreatic islets were isolated by collagenase digestion from male wild‐type and TRPM2‐knockout (KO) mice. Insulin release and nicotinamide adenine dinucleotide (NAD+) production in islets were measured under static incubation. NSCC currents in mouse single β‐cells were measured by patch‐clamp experiments. Results: Batch‐incubation studies showed that imeglimin enhanced GSIS at stimulatory 16.6 mM glucose, whereas it did not affect basal insulin levels at 2.8 mM glucose. Imeglimin increased the glucose‐induced production of NAD+, a precursor of cADPR, in islets and the insulinotropic effects of imeglimin were attenuated by a cADPR inhibitor 8‐Br‐cADPR. Furthermore, imeglimin increased NSCC current in β‐cells, and abolished this current in TRPM2‐KO mice. Imeglimin did not potentiate GSIS in the TRPM2‐KO islets, suggesting that imeglimin's increase of NSCC currents through the TRPM2 channel is causally implicated in its insulin releasing effects. Conclusions: Imeglimin may activate TRPM2 channels in β‐cells via the production of NAD+/cADPR, leading to the potentiation of GSIS. Developing approaches to stimulate cADPR‐TRPM2 signaling provides a potential therapeutic tool to treat type 2 diabetes. [ABSTRACT FROM AUTHOR]

Published
2022
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46. ELKS/Voltage-Dependent Ca²⁺ Channel-beta Subunit Module Regulates Polarized Ca²⁺ Influx in Pancreatic beta Cells

Author

Ohara-Imaizumi, Mica, Aoyagi, Kyota, Yamauchi, Hajime, Yoshida, Masashi, Mori, X., Masayuki, Hida, Yamato, Tran, Nam, Ha, Ohkura, Masamichi, Abe, Manabu, Akimoto, Yoshihiro, Nakamichi, Yoko, Nishiwaki, Chiyono, Kawakami, Hayato, Hara, Kazuo, Sakimura, Kenji, Nagamatsu, Shinya, Mori, Yasuo, Nakai, Junichi, Kakei, Masafumi, Ohtsuka, Toshihisa, Ohara-Imaizumi, Mica, Aoyagi, Kyota, Yamauchi, Hajime, Yoshida, Masashi, Mori, X., Masayuki, Hida, Yamato, Tran, Nam, Ha, Ohkura, Masamichi, Abe, Manabu, Akimoto, Yoshihiro, Nakamichi, Yoko, Nishiwaki, Chiyono, Kawakami, Hayato, Hara, Kazuo, Sakimura, Kenji, Nagamatsu, Shinya, Mori, Yasuo, Nakai, Junichi, Kakei, Masafumi, and Ohtsuka, Toshihisa

Published
2019

49. A new hypoglycemic agent, A-4166, inhibits ATP-sensitive potassium channels in rat pancreatic beta-cells

Author

Akiyoshi, Megumi, Kakei, Masafumi, Nakazaki, Mitsuhiro, and Tanaka, Hiromitsu

Subjects
Pancreatic beta cells -- Research, Potassium channels -- Research, Hypoglycemic agents -- Physiological aspects, Biological sciences
Abstract

Patch-clamp method-based study of beta-cells in rat pancreas reveals the presence of hypoglycemic drug, N-(trans-4-isopropylcyclohexy-carbonyl)-D-phenylalanine (A-4166), an ATP-sensitive K+ (K-ATP) channel inhibitor. The inhibitory action proceeds through insulin release stimulation from beta-cells and is more effective than tolbutamide-mediated inhibition. There is no change in single-channel conduction of the K-ATP channel.

Published
1995

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