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Your search keyword '"Junji Kamon"' showing total 2 results
Start Over Author "Junji Kamon" Journal nature medicine
2 results on '"Junji Kamon"'

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

Author

Takeshi Takazawa, Ryozo Nagai, Hitomi Ogata, Philippe Froguel, Masato Iwabu, Tomohiro Ide, Miki Okada-Iwabu, Tetsuya Kubota, Hideki Kozono, Kazuyuki Tobe, Iseki Takamoto, Yasunori Nio, Atsushi Tsuchida, Yusuke Hada, Masaki Tsunoda, Yusuke Ito, Junji Kamon, Kazuo Hara, Masaki Kobayashi, Toshiyuki Maki, Motoharu Awazawa, Kumpei Tokuyama, Kohjiro Ueki, Katsuyoshi Kumagai, Toshimasa Yamauchi, Naoto Kubota, Kouji Murakami, Sachiko Kawamoto, Takashi Kadowaki, Information génomique et structurale (IGS), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Génétique des maladies multifactorielles (GMM), Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), Section of Genomic Medicine, Imperial College London, Genome Centre, and Imperial College London-Hammersmith campus

Subjects
Blood Glucose, Male, Peroxisome proliferator-activated receptor, Mice, Obese, MESH: Gene Targeting, MESH: Mice, Knockout, chemistry.chemical_compound, Mice, 0302 clinical medicine, MESH: Diabetes Mellitus, Experimental, MESH: Animals, MESH: Mice, Obese, MESH: Receptors, Cell Surface, MESH: Lipid Metabolism, chemistry.chemical_classification, Adiponectin receptor 1, Mice, Knockout, 0303 health sciences, Adiponectin receptor 2, General Medicine, MESH: Adiponectin, AdipoRon, Gene Targeting, Receptors, Leptin, Female, Adiponectin, Receptors, Adiponectin, Protein Binding, medicine.medical_specialty, Adipokine, 030209 endocrinology & metabolism, Receptors, Cell Surface, Biology, General Biochemistry, Genetics and Molecular Biology, Diabetes Mellitus, Experimental, 03 medical and health sciences, MESH: Mice, Inbred C57BL, Internal medicine, medicine, MESH: Protein Binding, Animals, MESH: Mice, 030304 developmental biology, AMPK, Lipid Metabolism, MESH: Male, Mice, Inbred C57BL, Endocrinology, chemistry, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, MESH: Blood Glucose, Adiponectin binding, MESH: Female
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.

Published
2006
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2. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity

Author

Charles Vinson, Junji Kamon, Tomohiro Ide, Takashi Kadowaki, Kazuo Hara, Hiroyuki Kagechika, Kazuyuki Tobe, Y. Mori, Toshimasa Yamauchi, Koichi Shudo, Madoka Yoda, Yasuo Terauchi, Naoto Kubota, Motowo Tomita, R. Nagai, Philippe Froguel, Kouji Murakami, Hironori Waki, Osamu Ezaki, Yasuko Nakano, Shigeko Kimura, Marc L. Reitman, Nobuyo Tsuboyama-Kasaoka, Y. Akanuma, and Oksana Gavrilova

Subjects
Leptin, medicine.medical_specialty, Molecular Sequence Data, Receptors, Cytoplasmic and Nuclear, Biology, General Biochemistry, Genetics and Molecular Biology, chemistry.chemical_compound, Mice, Insulin resistance, Internal medicine, medicine, Animals, Adiponectin secretion, Amino Acid Sequence, Obesity, Triglycerides, Adiponectin receptor 1, Adiponectin receptor 2, Adiponectin, nutritional and metabolic diseases, Proteins, General Medicine, medicine.disease, AdipoRon, Endocrinology, chemistry, Adipose Tissue, Intercellular Signaling Peptides and Proteins, Metabolic syndrome, Insulin Resistance, Oxidation-Reduction, hormones, hormone substitutes, and hormone antagonists, Signal Transduction, Transcription Factors
Abstract

Adiponectin is an adipocyte-derived hormone. Recent genome-wide scans have mapped a susceptibility locus for type 2 diabetes and metabolic syndrome to chromosome 3q27, where the gene encoding adiponectin is located. Here we show that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. Adiponectin decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice. This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin and leptin, but only partially by either adiponectin or leptin alone. We conclude that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy. These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes.

Published
2001

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