Kazumasa Miyawaki
Kyoto University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Kazumasa Miyawaki.
Nature Medicine | 2002
Kazumasa Miyawaki; Yuichiro Yamada; Nobuhiro Ban; Yu Ihara; Katsushi Tsukiyama; Heying Zhou; Shimpei Fujimoto; Akira Oku; Kinsuke Tsuda; Shinya Toyokuni; Hiroshi Hiai; Wataru Mizunoya; Tohru Fushiki; Jens J. Holst; Mitsuhiro Makino; Akira Tashita; Yukari Kobara; Yoshiharu Tsubamoto; Takayoshi Jinnouchi; Takahito Jomori; Yutaka Seino
Secretion of gastric inhibitory polypeptide (GIP), a duodenal hormone, is primarily induced by absorption of ingested fat. Here we describe a novel pathway of obesity promotion via GIP. Wild-type mice fed a high-fat diet exhibited both hypersecretion of GIP and extreme visceral and subcutaneous fat deposition with insulin resistance. In contrast, mice lacking the GIP receptor (Gipr−/−) fed a high-fat diet were clearly protected from both the obesity and the insulin resistance. Moreover, double-homozygous mice (Gipr−/−, Lepob/Lepob) generated by crossbreeding Gipr−/− and obese ob/ob (Lepob/Lepob) mice gained less weight and had lower adiposity than Lepob/Lepob mice. The Gipr−/− mice had a lower respiratory quotient and used fat as the preferred energy substrate, and were thus resistant to obesity. Therefore, GIP directly links overnutrition to obesity and it is a potential target for anti-obesity drugs.
FEBS Letters | 2000
Yu Ihara; Yuichiro Yamada; Shinya Toyokuni; Kazumasa Miyawaki; Nobuhiro Ban; Tetsuya Adachi; Akira Kuroe; Toshio Iwakura; Akira Kubota; Hiroshi Hiai; Yutaka Seino
We have shown recently that oxidative stress by chronic hyperglycemia damages the pancreatic β‐cells of GK rats, a model of non‐obese type 2 diabetes, which may worsen diabetic condition and suggested the administration of antioxidants as a supportive therapy. To determine if natural antioxidant α‐tocopherol (vitamin E) has beneficial effects on the glycemic control of type 2 diabetes, GK rats were fed a diet containing 0, 20 or 500 mg/kg diet α‐tocopherol. Intraperitoneal glucose tolerance test revealed a significant increment of insulin secretion at 30 min and a significant decrement of blood glucose levels at 30 and 120 min after glucose loading in the GK rats fed with high α‐tocopherol diet. The levels of glycated hemoglobin A1c, an indicator of glycemic control, were also reduced. Vitamin E supplementation clearly ameliorated diabetic control of GK rats, suggesting the importance of not only dietary supplementation of natural antioxidants but also other antioxidative intervention as a supportive therapy of type 2 diabetic patients.
Diabetes | 2006
Yuichiro Yamada; Kazumasa Miyawaki; Katsushi Tsukiyama; Norio Harada; Chizumi Yamada; Yutaka Seino
The hormonal factor(s) implicated as transmitters of signals from the gut to pancreatic β-cells is referred to as incretin, and gastric inhibitory polypeptide (GIP) is identified as one of the incretins. GIP is a gastrointestinal peptide hormone of 42 amino acids that is released from duodenal endocrine K-cells after absorption of glucose or fat and exerts its effects by binding to its specific receptor, the GIP receptor. By generating and characterizing mice with a targeted mutation of the GIP receptor gene, we have shown that GIP has not only an insulinotropic role, but also physiological roles on fat accumulation into adipose tissues and calcium accumulation into bone. We here propose a new acronym, GIP, for gut-derived nutrient-intake polypeptide.
Biochemical and Biophysical Research Communications | 2008
Rei Naitoh; Kazumasa Miyawaki; Norio Harada; Wataru Mizunoya; Kentaro Toyoda; Tohru Fushiki; Yuichiro Yamada; Yutaka Seino; Nobuya Inagaki
Gastric inhibitory polypeptide (GIP) is an incretin and directly promotes fat accumulation in adipocytes. Inhibition of GIP signaling prevents onset of obesity and increases fat oxidation in peripheral tissues under high-fat diet (HFD), but the mechanism is unknown. In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr(-/-)) mice. In HFD-fed Gipr(-/-) mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. In addition, the PPARalpha mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr(-/-) mice compared with those in HFD-fed WT mice. These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD.
Diabetes Research and Clinical Practice | 2003
Fumiaki Sugawara; Yuichiro Yamada; Rie Watanabe; Nobuhiro Ban; Kazumasa Miyawaki; Akira Kuroe; Akihiro Hamasaki; Hiroki Ikeda; Takeshi Kurose; Masaru Usami; Masaki Ikeda; Yutaka Seino
TSC-22 is a leucine zipper transcriptional factor and expression of the TSC-22 gene is highly induced by TGF-beta treatment. We estimated the frequency of the -396 A/G polymorphism of the TSC-22 gene with an Alu I-Restriction fragment length polymorphism (RFLP) method in 498 Japanese subjects with type 2 diabetes mellitus. We also determined the promoter activity. The diabetic patients with the AA genotype had a significantly higher incidence of the diabetic nephropathy (vs. the AG genotype, P<0.05, odds ratio: 1.95; 95% confidence intervals 1.14-3.33). There was no significant difference in the promoter activity between the fragments with -396A and -396G. These findings suggest that the TSC-22 gene (-396) A allele is associated with an increasing risk of the diabetic nephropathy.
Journal of Diabetes Investigation | 2010
Kohtaro Minami; Kazumasa Miyawaki; Manami Hara; Shuichi Yamada; Susumu Seino
Aims/Introduction: Studies have suggested that pancreatic β‐cells undergo dedifferentiation during proliferation in vitro. However, due to limitations of the methodologies used, the question remains whether such dedifferentiated cells can redifferentiate into β‐cells.
Proceedings of the National Academy of Sciences of the United States of America | 1999
Kazumasa Miyawaki; Yuichiro Yamada; Hideki Yano; Hitoshi Niwa; Nobuhiro Ban; Yu Ihara; Akira Kubota; Shinpei Fujimoto; Mariko Kajikawa; Akira Kuroe; Kinsuke Tsuda; Hiroyuki Hashimoto; Tokuyuki Yamashita; Takahito Jomori; Fumi Tashiro; Jun-ichi Miyazaki; Yutaka Seino
Proceedings of the National Academy of Sciences of the United States of America | 2005
Kohtaro Minami; Masaaki Okuno; Kazumasa Miyawaki; Akinori Okumachi; Katsuhiko Ishizaki; Kazunobu Oyama; Miho Kawaguchi; Nobuko Ishizuka; Toshihiko Iwanaga; Susumu Seino
American Journal of Physiology-endocrinology and Metabolism | 2003
Nathalie Pamir; Francis C. Lynn; A.M.J. Buchan; Jan A. Ehses; Simon A. Hinke; J. Andrew Pospisilik; Kazumasa Miyawaki; Yuichiro Yamada; Yutaka Seino; Christopher H.S. McIntosh; Raymond A. Pederson
Biochemical and Biophysical Research Communications | 2005
Heying Zhou; Yuichiro Yamada; Katsushi Tsukiyama; Kazumasa Miyawaki; Masaya Hosokawa; Kazuaki Nagashima; Kentaro Toyoda; Rei Naitoh; Wataru Mizunoya; Tohru Fushiki; Takashi Kadowaki; Yutaka Seino