Cloning of adiponectin receptors that mediate antidiabetic metabolic effects

Toshimasa Yamauchi, Junji Kamon, Yusuke Ito, Atsushi Tsuchida, Takehiko Yokomizo, Shunbun Kita, Takuya Sugiyama, Makoto Miyagishi, Kazuo Hara, Masaki Tsunoda, Koji Murakami, Toshiaki Ohteki, Shoko Uchida, Sato Takekawa, Hironori Waki, Nelson H. Tsuno, Yoichi Shibata, Yasuo Terauchi, Philippe Froguel, Kazuyuki Tobe, Shigeo Koyasu, Kazunari Taira, Toshio Kitamura, Takao Shimizu, Ryozo Nagai and Takashi Kadowaki ()
Additional contact information
Toshimasa Yamauchi: University of Tokyo
Junji Kamon: University of Tokyo
Yusuke Ito: University of Tokyo
Atsushi Tsuchida: University of Tokyo
Takehiko Yokomizo: University of Tokyo
Shunbun Kita: University of Tokyo
Takuya Sugiyama: University of Tokyo
Makoto Miyagishi: University of Tokyo
Kazuo Hara: University of Tokyo
Masaki Tsunoda: Central Research Laboratories, Kyorin Pharmaceutical
Koji Murakami: Central Research Laboratories, Kyorin Pharmaceutical
Toshiaki Ohteki: CREST of Japan Science and Technology Corporation
Shoko Uchida: University of Tokyo
Sato Takekawa: University of Tokyo
Hironori Waki: University of Tokyo
Nelson H. Tsuno: University of Tokyo
Yoichi Shibata: University of Tokyo
Yasuo Terauchi: University of Tokyo
Philippe Froguel: Institute of Biology-CNRS, Pasteur Institute of Lille, UPRES
Kazuyuki Tobe: University of Tokyo
Shigeo Koyasu: CREST of Japan Science and Technology Corporation
Kazunari Taira: University of Tokyo
Toshio Kitamura: University of Tokyo
Takao Shimizu: University of Tokyo
Ryozo Nagai: University of Tokyo
Takashi Kadowaki: University of Tokyo

Nature, 2003, vol. 423, issue 6941, 762-769

Abstract: Abstract Corrigendum (2004) Adiponectin (also known as 30-kDa adipocyte complement-related protein; Acrp30)1,2,3,4 is a hormone secreted by adipocytes that acts as an antidiabetic5,6,7,8,9,10,11,12 and anti-atherogenic8,12,13 adipokine. Levels of adiponectin in the blood are decreased under conditions of obesity, insulin resistance and type 2 diabetes2. Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice5,6,7. Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes8,9. This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through activation of AMP kinase10,11 and PPAR-α5,6,12. Here we report the cloning of complementary DNAs encoding adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) by expression cloning14,15,16. AdipoR1 is abundantly expressed in skeletal muscle, whereas AdipoR2 is predominantly expressed in the liver. These two adiponectin receptors are predicted to contain seven transmembrane domains, but to be structurally and functionally distinct from G-protein-coupled receptors17,18,19. Expression of AdipoR1/R2 or suppression of AdipoR1/R2 expression by small-interfering RNA20 supports our conclusion that they serve as receptors for globular and full-length adiponectin, and that they mediate increased AMP kinase10,11 and PPAR-α ligand activities12, as well as fatty-acid oxidation and glucose uptake by adiponectin.

Date: 2003
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DOI: 10.1038/nature01705

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