Cited by 3,176Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismPeroxisome Proliferator-Activated Receptors

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Cloning of adiponectin receptors that mediate antidiabetic metabolic effects

Yamauchi, Toshimasa, Kamon, Junji, Ito, Yusuke, Tsuchida, Atsushi, Yokomizo, Takehiko, Kita, Shunbun, Sugiyama, Takuya, Miyagishi, Makoto, Hara, Kazuo, Tsunoda, Masaki, Murakami, Koji, Ohteki, Toshiaki, Uchida, Shoko, Takekawa, Sato, Waki, Hironori, Tsuno, Nelson H., Shibata, Yoichi, Terauchi, Yasuo, Froguel, Philippe, Tobe, Kazuyuki, Koyasu, Shigeo, Taira, Kazunari, Kitamura, Toshio, Shimizu, Takao, Nagai, Ryozo, Kadowaki, Takashi·2003·Nature

DOI 10.1038/nature01705

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Abstract

Adiponectin (also known as 30-kDa adipocyte complement-related protein; Acrp30) is a hormone secreted by adipocytes that acts as an antidiabetic and anti-atherogenic adipokine. Levels of adiponectin in the blood are decreased under conditions of obesity, insulin resistance and type 2 diabetes. Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice. Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes. This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through activation of AMP kinase and PPAR-alpha. Here we report the cloning of complementary DNAs encoding adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) by expression cloning. 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 receptors. Expression of AdipoR1/R2 or suppression of AdipoR1/R2 expression by small-interfering RNA supports our conclusion that they serve as receptors for globular and full-length adiponectin, and that they mediate increased AMP kinase and PPAR-alpha ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectin.

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Untitled work
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Authors: Yamauchi, T., Kamon, J., Ito, Y., Tsuchida, A., Yokomizo, T., Kita, S., Sugiyama, T., Miyagishi, M., Hara, K., Tsunoda, M., Murakami, K., Ohteki, T., Uchida, S., Takekawa, S., Waki, H., Tsuno, N. H., Shibata, Y., Terauchi, Y., Froguel, P., Tobe, K., Koyasu, S., Taira, K., Kitamura, T., Shimizu, T., Nagai, R., & Kadowaki, T.
Affiliations: The University of Tokyo (JP)
Nissan Chemical Corporation (Japan) (JP)
Japan Science and Technology Agency (JP)
National Institute of Advanced Industrial Science and Technology (JP)
Keio University (JP)
Centre National de la Recherche Scientifique (FR)
Institute of Medical Science, The University of Tokyo (JP)
Corresponding author: Kadowaki, Takashi
ORCID: Yamauchi, Toshimasa
Ito, Yusuke
Tsuchida, Atsushi
Yokomizo, Takehiko
Kita, Shunbun
Miyagishi, Makoto
Hara, Kazuo
Murakami, Koji
Ohteki, Toshiaki
Waki, Hironori
Tsuno, Nelson H.
Terauchi, Yasuo
Froguel, Philippe
Tobe, Kazuyuki
Koyasu, Shigeo
Kitamura, Toshio
Shimizu, Takao
Nagai, Ryozo
Kadowaki, Takashi
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2003-06-12
Volume: 423
Issue: 6941
Pages: 762-769
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature01705
OpenAlex: W1997978122
Cited by: 3,176
References: 28
Citations by year: 2026: 43 · 2025: 50 · 2024: 77 · 2023: 102 · 2022: 89 · 2021: 136 · 2020: 114 · 2019: 120 · 2018: 114 · 2017: 117 · 2016: 117 · 2015: 154 · 2014: 173 · 2013: 190 · 2012: 170
FWCI: 115.85
Type: journal article
Language: en
Update notices: erratum (2004-10-28)
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Novartis Foundation
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords: adiponectin, adiponectin receptors, AdipoR1, AdipoR2, insulin resistance, type 2 diabetes, AMP kinase, PPARα, fatty acid oxidation, glucose uptake, skeletal muscle, liver, adipokines, obesity, receptor cloning
MeSH terms: Amino Acid Sequence, Animals, Cell Line, Cloning, Molecular, Diabetes Mellitus, Endothelium, Vascular, Fatty Acids, Glucose, Humans, Hypoglycemic Agents, Ligands, Molecular Sequence Data, Oxidation-Reduction, Proteins, Receptors, Cell Surface, Transcription Factors, Receptors, Cytoplasmic and Nuclear, Hepatocytes, Muscle Cells, RNA Interference, RNA, Small Interfering, Intercellular Signaling Peptides and Proteins, Mice, Adiponectin, Receptors, Adiponectin

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Cloning of adiponectin receptors that mediate antidiabetic metabolic effects

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