Cardiac Metabolism in Health and Disease Dr. Rong Tian’s research interest is to understand the role of cardiac energy metabolism in the pathogenesis of cardiovascular diseases. Her laboratory utilizes multi-nuclei NMR spectroscopy to interrogate metabolic fluxes and myocardial energetics in animal models. Her current studies concentrate on myocardial substrate metabolism and metabolic signaling by combining the powerful NMR technique with her ability to target the molecular regulatory mechanisms via the genetic manipulation in animal models. Furthermore, Dr. Tian is also interested in bi-directional translational research between the bench and the bedside for elucidating the functional significance of altered cardiac metabolism in ischemic heart disease, obesity, diabetes and heart failure.
An adult human heart has the highest oxygen uptake rate in the body (~0.1ml O2/g/min at basal conditions); it generates and consumes about 6 Kg of ATP daily, 15-20 times of its own weight. Even though the heart has developed extensive metabolic machinery and sophisticated regulatory networks to ensure energy homeostasis, impairment of cardiac metabolism has been found in a variety of disease conditions. Importantly, the consequence of abnormal cardiac metabolism is no longer limited to deficient energy production, as the biological roles of mitochondria and reactive oxygen species have been increasingly recognized. Part of our current research aims at understanding the fundamental mechanisms linking altered myocardial substrate metabolism to cardiac dysfunction. This line of research seeks to generate a basis for metabolic therapy for heart failure and cardiac lipotoxicity in obesity and diabetes. Studies in this direction will also extend to nutrient-mediated gene expression and programming of the cardiovascular system. Another focus of our studies is metabolic signaling in cardiovascular biology. We were first to report an increased activity of AMP-activated protein kinase (AMPK), an energy sensor and master switch of metabolism, in hypertrophied hearts; and subsequently generated mice with cardiac-specific kinase-inactive AMPK. On-going investigations in the lab address novel roles of AMPK in mitochondria biogenesis/function, cell growth and insulin signaling.
Liao R, Jain M, Cui L, D’Agostino J, Aiello F, Ngoy S, Mortensen RM, Tian R. Cardiac-specific overexpression of GLUT1 prevents the development of heart failure due to pressure-overload in mouse. Circulation 2002, 106, 2125-2131.
Xing Y, Musi N, Fujii N, Zou L, Luptak I, Hirshman MF, Goodyear LJ, Tian R. Glucose metabolism and energy homeostasis in mouse hearts overexpressing dominant negative a2 subunit of AMP-activated protein kinase. J Biol Chem 2003, 278:28372-28377.
Zou L, Shen M, Arad M, He H, Lofgren B, Ingwall JS, Seidman CE, Seidman JG, Tian R. N488I mutation of the g2-subunit results in bi-directional changes in AMPK activity. Circ Res 2005 97(4):323-328.
Luptak I, Balschi JA, Xing Y, Leone TC, Kelly DP, Tian R. Decreased contractile reserve in PPARa-null hearts can be rescued by increasing glucose transport and utilization. Circulation 2005; 112:2339-2346.
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