G
Genichi Atsumi
Researcher at Harvard University
Publications - 4
Citations - 1247
Genichi Atsumi is an academic researcher from Harvard University. The author has contributed to research in topics: Metabolic syndrome & Insulin receptor. The author has an hindex of 3, co-authored 4 publications receiving 1158 citations. Previous affiliations of Genichi Atsumi include Teikyo University.
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Journal ArticleDOI
Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2
Masato Furuhashi,Gurol Tuncman,Cem Z. Görgün,Liza Makowski,Liza Makowski,Genichi Atsumi,Genichi Atsumi,Eric Vaillancourt,Keita Kono,Vladimir R. Babaev,Sergio Fazio,MacRae F. Linton,Richard B. Sulsky,Jeffrey A. Robl,Rex A. Parker,Gökhan S. Hotamisligil +15 more
TL;DR: It is demonstrated that an orally active small-molecule inhibitor of aP2 is an effective therapeutic agent against severe atherosclerosis and type 2 diabetes in mouse models and can lead to a new class of powerful therapeutic agents to prevent and treat metabolic diseases such as type 2 diabetes and atheros sclerosis.
Journal ArticleDOI
Adipocyte/macrophage fatty acid binding proteins control integrated metabolic responses in obesity and diabetes
Kazuhisa Maeda,Haiming Cao,Keita Kono,Cem Z. Görgün,Masato Furuhashi,Kadir T. Uysal,Qiong Cao,Genichi Atsumi,Harry Malone,Bala Krishnan,Yasuhiko Minokoshi,Barbara B. Kahn,Rex A. Parker,Gökhan S. Hotamisligil +13 more
TL;DR: It is demonstrated that adipocyte/macrophage FABPs have a robust impact on multiple components of metabolic syndrome, integrating metabolic and inflammatory responses in mice and constituting a powerful target for the treatment of these diseases.
Journal ArticleDOI
Role of the Fatty Acid Binding Protein mal1 in Obesity and Insulin Resistance
Kazuhisa Maeda,K. Teoman Uysal,Liza Makowski,Cem Z. Görgün,Genichi Atsumi,Rex A. Parker,Jens C. Brüning,Ann V. Hertzel,David A. Bernlohr,Gökhan S. Hotamisligil +9 more
TL;DR: It is demonstrated that mal1 modulates adipose tissue function and contributes to systemic glucose metabolism and constitutes a potential therapeutic target in insulin resistance.