J
Junji Kamon
Researcher at University of Tokyo
Publications - 28
Citations - 19299
Junji Kamon is an academic researcher from University of Tokyo. The author has contributed to research in topics: Adiponectin & Insulin resistance. The author has an hindex of 19, co-authored 28 publications receiving 18459 citations.
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Journal ArticleDOI
The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity
Toshimasa Yamauchi,Junji Kamon,Hironori Waki,Yasuo Terauchi,Naoto Kubota,Kazuo Hara,Y. Mori,Tomohiro Ide,Kouji Murakami,Nobuyo Tsuboyama-Kasaoka,Osamu Ezaki,Y. Akanuma,Oksana Gavrilova,Charles Vinson,Marc L. Reitman,Hiroyuki Kagechika,Koichi Shudo,Madoka Yoda,Yasuko Nakano,Kazuyuki Tobe,R. Nagai,Shigeko Kimura,Motowo Tomita,Philippe Froguel,Takashi Kadowaki +24 more
TL;DR: It is concluded that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy and that the replenishment of adiponECTin might provide a novel treatment modality for insulin resistance and type 2 diabetes.
Journal ArticleDOI
Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase
Toshimasa Yamauchi,Junji Kamon,Yasuhiko Minokoshi,Yoichi M. Ito,Hironori Waki,S. Uchida,Shigeo Yamashita,Mitsuhiko Noda,Shunbun Kita,K Ueki,Koji Eto,Y. Akanuma,Philippe Froguel,Fabienne Foufelle,Pascal Ferré,David Carling,Shigeko Kimura,Ryozo Nagai,Barbara B. Kahn,Takashi Kadowaki +19 more
TL;DR: It is shown that phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full- lengths Ad in the liver, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK.
Journal ArticleDOI
Cloning of adiponectin receptors that mediate antidiabetic metabolic effects
Toshimasa Yamauchi,Junji Kamon,Yusuke Ito,Atsushi Tsuchida,Takehiko Yokomizo,Takehiko Yokomizo,Shunbun Kita,Takuya Sugiyama,Makoto Miyagishi,Makoto Miyagishi,Kazuo Hara,Masaki Tsunoda,Koji Murakami,Toshiaki Ohteki,S. Uchida,Sato Takekawa,Hironori Waki,Nelson H. Tsuno,Yoichi Shibata,Yasuo Terauchi,Philippe Froguel,Kazuyuki Tobe,Shigeo Koyasu,Kazunari Taira,Kazunari Taira,Toshio Kitamura,Takao Shimizu,Takao Shimizu,Ryozo Nagai,Takashi Kadowaki +29 more
TL;DR: The cloning of complementary DNAs encoding adiponectin receptors 1 and 2 by expression cloning supports the conclusion that they serve as receptors for globular and full-length adiponECTin, and that they mediate increased AMP kinase and PPAR-α ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectionin.
Journal ArticleDOI
Disruption of adiponectin causes insulin resistance and neointimal formation.
Naoto Kubota,Yasuo Terauchi,Toshimasa Yamauchi,Tetsuya Kubota,Masao Moroi,Junji Matsui,Kazuhiro Eto,Tokuyuki Yamashita,Junji Kamon,Hidemi Satoh,Wataru Yano,Philippe Froguel,Ryozo Nagai,Satoshi Kimura,Takashi Kadowaki,Tetsuo Noda,Tetsuo Noda +16 more
TL;DR: This study provides the first direct evidence that adiponectin plays a protective role against insulin resistance and atherosclerosis in vivo.
Journal ArticleDOI
Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions.
Toshimasa Yamauchi,Yasunori Nio,Toshiyuki Maki,Masaki Kobayashi,Takeshi Takazawa,Masato Iwabu,Miki Okada-Iwabu,Sachiko Kawamoto,Naoto Kubota,Tetsuya Kubota,Yusuke Ito,Junji Kamon,Atsushi Tsuchida,Katsuyoshi Kumagai,Hideki Kozono,Yusuke Hada,Hitomi Ogata,Kumpei Tokuyama,Masaki Tsunoda,Tomohiro Ide,Kouji Murakami,Motoharu Awazawa,Iseki Takamoto,Philippe Froguel,Kazuo Hara,Kazuyuki Tobe,Ryozo Nagai,Kohjiro Ueki,Takashi Kadowaki +28 more
TL;DR: Adenovirus-mediated expression of AdipoR1 and R2 in the liver of Lepr−/− mice increased AMP-activated protein kinase (AMPK) activation and peroxisome proliferator-activated receptor (PPAR)-α signaling pathways, respectively, and abolished adiponectin binding and actions, leading to insulin resistance and marked glucose intolerance in vivo.