Cited by 844Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and Metabolism

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Adiponectin Stimulates AMP-Activated Protein Kinase in the Hypothalamus and Increases Food Intake

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Kubota, Naoto, Yano, Wataru, Kubota, Tetsuya, Yamauchi, Toshimasa, Itoh, Shinsuke, Kumagai, Hiroki, Kozono, Hideki, Takamoto, Iseki, Okamoto, Shiki, Shiuchi, Tetsuya, Suzuki, Ryo, Satoh, Hidemi, Tsuchida, Atsushi, Moroi, Masao, Sugi, Kaoru, Noda, Tetsuo, Ebinuma, Hiroyuki, Ueta, Yoichi, Kondo, Tatsuya, Araki, Eiichi, Ezaki, Osamu, Nagai, Ryozo, Tobe, Kazuyuki, Terauchi, Yasuo, Ueki, Kohjiro, Minokoshi, Yasuhiko, Kadowaki, Takashi·2007·Cell Metabolism

DOI 10.1016/j.cmet.2007.06.003

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Abstract

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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Authors: Kubota, N., Yano, W., Kubota, T., Yamauchi, T., Itoh, S., Kumagai, H., Kozono, H., Takamoto, I., Okamoto, S., Shiuchi, T., Suzuki, R., Satoh, H., Tsuchida, A., Moroi, M., Sugi, K., Noda, T., Ebinuma, H., Ueta, Y., Kondo, T., Araki, E., Ezaki, O., Nagai, R., Tobe, K., Terauchi, Y., Ueki, K., Minokoshi, Y., & Kadowaki, T.
Affiliations: Japan Science and Technology Agency (JP)
The University of Tokyo (JP)
Toho University (JP)
National Institute for Physiological Sciences (JP)
Tohoku University (JP)
University of Occupational and Environmental Health Japan (JP)
Kumamoto University (JP)
Yokohama City University (JP)
Corresponding author: Kadowaki, Takashi
ORCID: Kubota, Naoto
Yano, Wataru
Kubota, Tetsuya
Yamauchi, Toshimasa
Itoh, Shinsuke
Okamoto, Shiki
Shiuchi, Tetsuya
Suzuki, Ryo
Tsuchida, Atsushi
Moroi, Masao
Ueta, Yoichi
Kondo, Tatsuya
Araki, Eiichi
Ezaki, Osamu
Nagai, Ryozo
Tobe, Kazuyuki
Terauchi, Yasuo
Ueki, Kohjiro
Minokoshi, Yasuhiko
Kadowaki, Takashi
Venue: Cell Metabolism
Publisher: Elsevier BV
Published: 2007-07
Volume: 6
Issue: 1
Pages: 55-68
ISSN: 1550-4131 (ISSN-L)
DOI: 10.1016/j.cmet.2007.06.003
OpenAlex: W2128485668
Cited by: 844
References: 37
Citations by year: 2026: 24 · 2025: 26 · 2024: 26 · 2023: 46 · 2022: 36 · 2021: 54 · 2020: 37 · 2019: 36 · 2018: 42 · 2017: 34 · 2016: 59 · 2015: 31 · 2014: 56 · 2013: 54 · 2012: 53
FWCI: 22.05
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 2208 d)
Locations: Cell Metabolism (publishedVersion)
PubMed (publishedVersion)
Funders: Ministry of Education, Culture, Sports, Science and Technology
Ministry of Health and Welfare
Juvenile Diabetes Research Foundation International (1-2003-746)
Daiichi Sankyo Foundation of Life Science
Astellas Foundation for Research on Metabolic Disorders
Kanae Foundation for the Promotion of Medical Science
Japan Society for the Promotion of Science (10NP0201)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords: adiponectin, AMPK, arcuate nucleus, hypothalamus, dietary intake, energy expenditure, AdipoR1, fasting, refeeding, high-fat diet-induced obesity, central nervous system
MeSH terms: Adenoviridae, Animals, Arcuate Nucleus of Hypothalamus, Eating, Energy Metabolism, Female, Hypothalamus, Immunoenzyme Techniques, Male, Mice, Inbred C57BL, Multienzyme Complexes, Phosphorylation, Receptors, Cell Surface, RNA Probes, Protein Serine-Threonine Kinases, In Situ Hybridization, Mice, Knockout, Leptin, Mice, Adiponectin, Adipose Tissue, White, Receptors, Leptin, Receptors, Adiponectin, AMP-Activated Protein Kinases

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Adiponectin Stimulates AMP-Activated Protein Kinase in the Hypothalamus and Increases Food Intake

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