Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake

Naoto Kubota, Wataru Yano, Tetsuya Kubota, Toshimasa Yamauchi, Shinsuke Itoh, Hiroki Kumagai, Hideki Kozono, Iseki Takamoto, Shiki Okamoto, Tetsuya Shiuchi, Ryo Suzuki, Hidemi Satoh, Atsushi Tsuchida, Masao Moroi, Kaoru Sugi, Tetsuo Noda, Hiroyuki Ebinuma, Yoichi Ueta, Tatsuya Kondo, Eiichi Araki, Osamu Ezaki, Ryozo Nagai, Kazuyuki Tobe, Yasuo Terauchi, Kohjiro Ueki, Yasuhiko Minokoshi, Takashi Kadowaki
Cell Metabolism 2007, 6 (1): 55-68
Adiponectin has been shown to stimulate fatty acid oxidation and enhance insulin sensitivity through the activation of AMP-activated protein kinase (AMPK) in the peripheral tissues. The effects of adiponectin in the central nervous system, however, are still poorly understood. Here, we show that adiponectin enhances AMPK activity in the arcuate hypothalamus (ARH) via its receptor AdipoR1 to stimulate food intake; this stimulation of food intake by adiponectin was attenuated by dominant-negative AMPK expression in the ARH. Moreover, adiponectin also decreased energy expenditure. Adiponectin-deficient mice showed decreased AMPK phosphorylation in the ARH, decreased food intake, and increased energy expenditure, exhibiting resistance to high-fat-diet-induced obesity. Serum and cerebrospinal fluid levels of adiponectin and expression of AdipoR1 in the ARH were increased during fasting and decreased after refeeding. We conclude that adiponectin stimulates food intake and decreases energy expenditure during fasting through its effects in the central nervous system.

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