Mitsuharu OKUTSU

Mitsuharu OKUTSU

Lecturer, Ph.D.
E-mail: okutsu
TEL: +81-52-872-5837
Research Course: Biological Science
URL http://www.nsc.nagoya-cu.ac.jp/~okutsu/  
Specialties Molecular Biology and Cellular Physiology of Exercise
Keywords skeletal muscle, atherosclerosis, exercise
Current Research (1) How to prevent against cachectic factor-induced skeletal muscle atrophy:
Cachectic factor induces skeletal muscle atrophy. Exercise training prevents against skeletal muscle atrophy, however, little is known about the underlying mechanisms. A goal in our lab is to establish the factor “X” to prevent against skeletal muscle atrophy.

(2) Molecular mechanism of prevention against atherosclerosis by exercise:
Exercise training prevents the development of atherosclerosis. Our goal in this project is to identify and determine the molecular mechanism in exercise-induced protection of endothelial cell damage (dysfunction) in atherosclerosis.
Selected Papers Extracellular superoxide dismutase ameliorates skeletal muscle abnormalities, cachexia and exercise intolerance in mice with congestive heart failure. Circulation: Heart Failure (in press)

Exercise prevents maternal high-fat diet-induced hypermethylation of the Pgc-1α gene and age-dependent metabolic dysfunction in the offspring. Diabetes (in press)

Corticosterone accelerates atherosclerosis in the apolipoprotein E-deficient mouse. Atherosclerosis, 232, 414-9 (2014).

Autophagy is required for exercise training-induced skeletal muscle adaptation and improvement of physical performance. FASEB Journal, 27, 4184-93 (2013).

Baf60c drives glycolytic metabolism in the muscle and improves systemic glucose homeostasis through Deptor-mediated Akt activation. Nature Medicine, 19, 640-5 (2013).

A novel PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell, 151, 1319-31 (2012).

Exercise training enhances in vivo tuberculosis purified protein derivative response in the elderly. Journal of Applied Physiology, 104, 1690-6 (2008).

Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress. American Journal of Physiology - Regulatory Integrative and Comparative Physiology, 288, R591-9 (2005).