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. 2007 Mar;13(3):332-9.
doi: 10.1038/nm1557. Epub 2007 Feb 1.

Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions

Toshimasa Yamauchi  1 , 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
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Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions

Toshimasa Yamauchi et al. Nat Med. 2007 Mar.

Abstract

Adiponectin plays a central role as an antidiabetic and antiatherogenic adipokine. AdipoR1 and AdipoR2 serve as receptors for adiponectin in vitro, and their reduction in obesity seems to be correlated with reduced adiponectin sensitivity. Here we show that 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)-alpha signaling pathways, respectively. Activation of AMPK reduced gluconeogenesis, whereas expression of the receptors in both cases increased fatty acid oxidation and lead to an amelioration of diabetes. Alternatively, targeted disruption of AdipoR1 resulted in the abrogation of adiponectin-induced AMPK activation, whereas that of AdipoR2 resulted in decreased activity of PPAR-alpha signaling pathways. Simultaneous disruption of both AdipoR1 and R2 abolished adiponectin binding and actions, resulting in increased tissue triglyceride content, inflammation and oxidative stress, and thus leading to insulin resistance and marked glucose intolerance. Therefore, AdipoR1 and R2 serve as the predominant receptors for adiponectin in vivo and play important roles in the regulation of glucose and lipid metabolism, inflammation and oxidative stress in vivo.

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