M
Masato Kasuga
Researcher at Kobe University
Publications - 506
Citations - 41710
Masato Kasuga is an academic researcher from Kobe University. The author has contributed to research in topics: Insulin receptor & Insulin. The author has an hindex of 96, co-authored 500 publications receiving 39782 citations. Previous affiliations of Masato Kasuga include Stanford University & Showa University.
Papers
More filters
Journal ArticleDOI
MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity
Hajime Kanda,Sanshiro Tateya,Yoshikazu Tamori,Ko Kotani,Ko Kotani,Kenichi Hiasa,Riko Kitazawa,Sohei Kitazawa,Hitoshi Miyachi,Sakan Maeda,Kensuke Egashira,Masato Kasuga +11 more
TL;DR: It is suggested that an increase in MCP-1 expression in adipose tissue contributes to the macrophage infiltration into this tissue, insulin resistance, and hepatic steatosis associated with obesity in mice.
Journal Article
Report of the committee on the classification and diagnostic criteria of diabetes mellitus (revision for international harmonization of HbAle in Japan)
Yoshiki Seino,Kishio Nanjo,Naoko Tajima,Takashi Kadowaki,Atsunori Kashiwagi,Eiichi Araki,Chikako Ito,Nobuya Inagaki,Yasuhiko Iwamoto,Masato Kasuga,Toshiaki Hanafusa,Masakazu Haneda,Kohjiro Ueki +12 more
TL;DR: Diabetes mellitus is a group of diseases associated with various metabolic disorders, the main feature of which is chronic hyperglycemia due to insufficient insulin action, which can cause susceptibility to specific complications and also foster arteriosclerosis.
Journal ArticleDOI
Report of the Committee on the Classification and Diagnostic Criteria of Diabetes Mellitus
Yutaka Seino,Kishio Nanjo,Naoko Tajima,Takashi Kadowaki,Atsunori Kashiwagi,Eiichi Araki,Chikako Ito,Nobuya Inagaki,Yasuhiko Iwamoto,Masato Kasuga,Toshiaki Hanafusa,Masakazu Haneda,Kohjiro Ueki +12 more
TL;DR: The concept of diabetes mellitus as mentioned in this paper is a group of diseases associated with various metabolic disorders, the main feature of which is chronic hyperglycemia due to insufficient insulin action.
Journal ArticleDOI
Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin.
Akihiro Asakawa,Akio Inui,Toshihiro Kaga,Hideki Yuzuriha,Toshiaki Nagata,Naohiko Ueno,Susumu Makino,Mineko Fujimiya,Akira Niijima,Masayuki A. Fujino,Masato Kasuga +10 more
TL;DR: Ghrelin, which is negatively regulated by leptin and IL-1 beta, is secreted by the stomach and increases arcuate NPY expression, which in turn acts through Y(1) receptors to increase food intake and decrease energy expenditure.
Journal ArticleDOI
Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1.
Hiroyuki Tamemoto,Takashi Kadowaki,Kazuyuki Tobe,Takeshi Yagi,Hiroshi Sakura,Takaki Hayakawa,Takaki Hayakawa,Yasuo Terauchi,Kohjiro Ueki,Yasushi Kaburagi,Shinobu Satoh,Hisahiko Sekihara,Shinji Yoshioka,Hiroyoshi Horikoshi,Yasuhide Furuta,Yoji Ikawa,Masato Kasuga,Yoshio Yazaki,Shinichi Aizawa +18 more
TL;DR: The data suggest that mice homozygous for targeted disruption of the IRS-1 gene were born alive but were retarded in embryonal and postnatal growth and the exis-tence of both IRS- 1-dependent and IRS-2-independent pathways for signal transduction of insulin and IGFs is suggested.