• Text in Japanese

Molecular analysis of metabolic syndrome and adiponectin, which were discovered by the lab, and new medical application

High blood sugar, high blood pressure, and low HDL are all associated with ill health, but none of these will cause death. Atherosclerosis is, however, a serious risk if a patient shows the above indications, and is associated with obesity, especially visceral fat. We are researching the relationship between visceral fat and atherosclerosis, which led to the discovery and functional study of adiponectin. This research has led us to propose the concepts of visceral fat syndrome and metabolic syndrome. We are studying these syndromes using basic and clinical research with aim of understanding their pathogenesis [1-19]. With adiponectin at its basis, our work has identified and characterized various molecules related to the onset and development of metabolic syndrome [20-23]. In addition, we are investigating adipose tissue and its role in disease. We have termed this field of research, ""adipo science"", which covers the study of adipose tissue, metabolism, atherosclerosis and chronic organ failure. [24, 25].

Schematic illustration of pathophysiology in metabolic syndrome

For well over a decade now, the medical community has been alarmed at the extraordinary increase in type 2 diabetes, which is associated with obesity. Recent research of patients in the West has correlated the risk of developing type 2 diabetes with a BMI over 25. This tendency is true for over half of patients in Japan as well. The rise of type 2 diabetes has directed large amounts of research to the molecular mechanisms regulating metabolic syndrome and related medical application.

[References]

1. Maeda et al. Nat Med 8(7):731-7, 2002.
2. Maeda et al. Nat Clin Pract Endocrinol Metab 4(11):627-34, 2008.
3. Maeda et al. PNAS 101(51):17801-6, 2004.
4. Hibuse et al. PNAS 102(31):10993-8, 2005.
5. Maeda et al. Diabetes 50(9):2094-9, 2001.
6. Kuriyama et al. Diabetes 51(10):2915-21, 2002.
7. Iwaki et al. Diabetes 52(7):1655-63, 2003.
8. Kumada et al. Circulation 109(17):2046-9, 2004.
9. Imanishi et al. Circulation 124(11 Suppl):S10-7, 2011.
10. Ohashi et al. JACC 43(7):1195-200, 2004.
11. Tsukamoto et al. JACC 53(22):2070-7, 2009.
12. Fujishima et al. FASEB J 2017.
13. Bauche et al. Endocrinology 148(4):1539-49, 2007.
14. Jortay et al. Endocrinology 151(10):4840-51, 2010.
15. Matsuda et al. Endocrinology 156(3):934-46, 2015.
16. Hiuge et al. ATVB 27(3):635-41, 2007.
17. Fujita et al. ATVB 28(5):863-70, 2008.
18. Kondo et al. JBC 284(3):1718-24, 2009.
19. Mori et al. Sci Rep 4:4895, 2014.
20. Sekimoto et al. PNAS 112(16):E2058-66, 2015.
21. Hiuge-Shimizu et al. ATVB 31(4):792-9, 2011.
22. Mori et al. PLoS One 8(10):e76199, 2013.
23. Inoue et al. PLoS One 9(2):e87661, 2014.