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 - Clinical Medicine (Core Departments) - Internal Medicine
Diabetes and Clinical Nutrition
The department of Diabetes and Clinical Nutrition was founded as the Nutritional Care Unit of Kyoto University Hospital in 1933, and became the division of Clinical Nutrition in 1981 as a central clinical facility. In 1992, the department was reestablished to reflect its academic and scientific roles of providing advanced instruction to medical students in the roles of metabolism and nutrition as well as research opportunities for graduates students in diabetology and nutritional research. We are very active in research and publication, and we encourage ambitious students to consider joining us.

  Nobuya Inagaki, M.D., Ph.D.
Research and Education
Our major interest is to clarify the mechanisms of the onset of metabolic disease, especially diabetes mellitus. Our studies include the production and secretion of insulin in pancreatic Beta-cells (Fig.1), secretion and action of the incretins such as GIP and GLP-1 (Fig.2), development of Beta-cell imaging, pathophysiological and genetic studies of diabetes mellitus, metabolism in Beta-cell and liver, transplantation of pancreatic Beta-cells, clinical study of diabetic mellitus and nutritional disorders, and development of stimulation system of energy metabolism. For example, we recently have shown that gastrointestinal polypeptide secreted in the duodenum plays a critical role in the maintenance of glycemic homeostasis and succeeded in islet transplantation from a living donor .
Each research project is independent, and all graduate students are allowed freedom to pursue their interest. The teaching staff contributes timely encouragement, discussion, and advice, and teaches the practical techniques required to carry out the experiments. We investigate physiology, pathology, and molecular and cellular biology using animal models and the most advanced analytical methods. During the course of the research, the student learns the numerous skills required for systematic analysis and scientific decision making.

Diabetes and Clinical Nutrition
Professor Nobuya Inagaki

Kazuaki Nagashima,
Kentaro Toyoda
Senior Lecturer
(Special Appointment):Shin-ichi Harashima
Akihiro Hamasaki,
Norio Harada,
Yoshihito Fujita
Shunsuke Yamane,
Masahito Ogura,
Daisuke Tanaka,
Tomoaki Osugi,
Yasuhiko Nakamura,
Hiroyuki Fujimoto
The mechanism of insulin secretion.The figure indicates the mechanism of insulin secretion from pancreatic beta cells by the stimulation of glucose or hypoglycemic agents. Several agents use in the treatment of diabetic patients are the target of our research.
The roles of incretin in glycemic homeostasis.Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the physiological incretin that stimulates insulin release upon ingestion of nutrients. To clarify the roles of these hormones in the maintenance of glycemic homeostasis, we are carrying out various experiments using various gene targeting mice.
The research meeting.Graduate students make a presentation about their experimental data in English.
The clinical conference is held once a week.We discuss about the problems in each patient.
The scene on experiment. Each graduate student has some independent research projects and teaching-stuffs advise timely.
Recent Publications
1. Inagaki N. et al. Reconstitution of IATP: an inward rectifier subunit plus the sulfonylurea receptor. Science. 1995: 270(5239):1166-70
2. Yamada K, Inagaki N. et al. A real-time method of imaging glucose uptake in single, living mammalian cells. Nat. Protoc. 2007: 2(3)753-62
3. Fujita Y, Inagaki N. Metformin suppresses hepatic gluconeogenesis and lowers fasting blood glucose levels through reactive nitrogen species in mice. Diabetologia. 2010: 53(7):1472-81.
4. Yoshihara E, Inagaki N, et al. Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity. Nat Commun. 2010: 1(8):127.
5. Mukai E, Inagaki N. et al. Exendin-4 suppresses SRC activation and reactive oxygen species production in diabetic Goto-Kakizaki rat islets in an Epac-dependent manner. Diabetes. 2011: 60(1):218-26.
6. Ikeda K, Inagaki N. et al. Impact of endogenous and exogenous insulin on basal energy expenditure in patients with type 2 diabetes under standard treatment. Am. J. Clin. Nutr 2011: 94: 1513-1518.