Untitled Document

Research

Kurt M. Saupe

Ph.D., University of Wisconsin-Madison
Assistant Professor, Department of Medicine, Cardiovascular Division
kws@medicine.wisc.edu
http://www2.medicine.wisc.edu/home/people-search/people/staff/2358/SAUPE_KURT_W/

Myocardial Pathophysiology and Metabolism

My laboratory conducts studies on myocardial pathophysiolgy in general, with a focus on myocardial metabolism. Our current research has two main components. The first is the study of myocardial energy metabolism; how it changes with normal aging, exercise training, and diseases such as heart failure, diabetic cardiomyopathy and ischemic heart disease. The overall goal of this research is to improve understanding of the biochemistry of myocardial metabolism, allowing therapeutic manipulation of myocardial metabolism. We are particularly interested in investigating the mechanism(s) by which increasing the amount of glucose and insulin provided to the ischemic heart is cardioprotective. We also focus on an important enzyme in maintenance of cardiac energy stores, AMP-activated protein kinase. My other research investigates the causes of exercise intolerance in heart disease.

These studies investigate the molecular and biochemical mechanisms of exercise intolerance in animal models of heart failure of varying etiologies. Upon determining contributing causes to exercise intolerance, the major goal is to develop targeted pharmacological and non-pharmacological interventions that may improve exercise tolerance. The experimental models we use are primarily rat models of acute and chronic heart failure, as well as young and old transgenic and wildtype mice. We are always looking for energetic individuals at all levels who are interested in joining our laboratory group.

Representative Publications
Barger, J.L., Kayo, T., Vann, J.M., Arias, E.B., Wang, J., Hacker, T.A., Wang, Y., Raederstorff, D., Morrow, J.D., Leeuwenburgh, C., Allison, D.B., Saupe, K.W., Cartee, G.D., Weindruch, R., & Prolla, T.A. (2008). A low dose of dietary resveratrol partially mimics caloric restriction and retards aging parameters in mice. PLoS ONE, 3(6), e2264.

Mulligan, J.D., Stewart, A.M., & Saupe, K.W. (2008). Downregulation of plasma insulin levels and hepatic PPAR? expression during the first week of caloric restriction in mice. Experimental Gerontology, 43(3), 146-153.

Mulligan, J.D., Gonzalez, A.A., Stewart, A.M., Carey, H.V., & Saupe, K.W. (2007). Upregulation of AMPK during cold exposure occurs via distinct mechanism in brown and white adipose tissue. J. Physiol., 580(Pt. 2), 677-84.

Colman, R.J., Nam, G., Huchthausen, L., Mulligan, J.D., & Saupe, K.W. (2007). Energy restriction-induced changes in body composition are age specific in mice. J. Nutrition, 137(10), 2247-51.

Saupe, K.W., & Mulligan, J.D. (2007). Beyond treating obesity: the anti-aging effects of caloric restriction. In D. Bagchi, & H.G. Preuss (Eds.), Obesity: Epidemiology, pathophysiology & prevention (pp. 265-272). CRC Press.

Korzick, D.H., Kostyak, J.C., Hunter, J.C., & Saupe, K.W. (2007). Local delivery of PKC?-activating peptide mimics ischemic preconditioning in aged hearts through GSK3? but not F1ATPase inactivation. Am. J. Physiol. Heart Circ. Physiol., 293(4), H2056-63.

Mulligan, J.D., Gonzalez, A.A., Kumar, R., Davis, A.J., & Saupe, K.W. (2005). Aging elevates basal AMPK activity and eliminates hypoxic activation of AMPK in mouse liver. Journal of Gerontology, 60A, 121-27.

Gonzalez, A.A., Kumar, R., Mulligan, J.D., Davis, A.J., & Saupe, KW. (2004). Effects of aging on cardiac and skeletal muscle AMPK activity: basal activity, allosteric activation, and response to in vivo hypoxemia in mice. Am. J. Physiol. Regul. Integr. Comp. Physiol., 287(5), R1270-5.

Gonzalez, A.A., Kumar, R., Mulligan, J.D., Davis, A.J., Weindruch, R., & Saupe, K.W. (2004). Metabolic adaptations to fasting and chronic caloric restriction in heart, muscle, and liver do not include changes in AMPK activity. Am. J. Physiol. Endocrinol. Metab., 287(5), E1032-7.

Koh, S.G., Brenner, D.A., Korzick, D.H., Tickerhoof, M., Apstein, C.S., & Saupe, K.W. (2003). Exercise intolerance during post-MI heart failure in rats: Prevention with supplemental dietary propionyl-L-carnitine. Cardiovascular Drugs and Therapy, 17(1), 7-14.

Saupe, K.W., Sobol, S.C., Koh, S.G., & Apstein, C.S. (2003). Effects of AT1 block begun late in life on normal cardiac aging in rats. J. Cardiovascular Pharmacology, 42(4), 573-580.

Guazzi, M., Brenner, D.A., Apstein, C.S., & Saupe, K.W. (2001). Exercise intolerance in rats with hypertensive heart disease is associated with impaired diastolic relaxation. Hypertension, 37, 204-208.

Saupe, K.W., Eberli, F.R., Ingwall, J.S., & Apstein, C.A. (2001). Metabolic support as an adjunct to inotropic support in the hypoperfused heart. J. Mol. Cell Cardiol., 33(2), 261-269.

Brenner, D., Apstein, C.S., & Saupe, K.W. (2001). Exercise training attenuates age-associated diastolic dysfunction in rats. Circulation, 104, 221-226.

Shen, W., Tian, R., Saupe, K.W., Spindler, M., & Ingwall, J.S. (2001). Endogenous nitric oxide enhances the coupling between O2 consumption and ATP synthesis in the guinea pig heart. Am. J. Physiol. Heart Circ. Physiol., 281, H838-H846.

Cave, A.C., Ingwall, J.S., Friedrich, J., Liao, R., Saupe, K.W., Apstein, C.S., & Eberli, F.R. (2000). ATP synthesis during low-flow ischemia: influence of increased glycolytic substrate. Circulation, 101(17), 2090-2096.

Saupe, K.W., Lim, C.C., Ingwall, J.S., Apstein, C.S., & Eberli, F.R. (2000). Comparison of hearts with 2 types of pressure-overload left ventricular hypertrophy. Hypertension, 35(5), 1167-1172, 2000.

Saupe, K.W., Spindler, M., Hopkins, J.C., Shen, W., & Ingwall, J.S. (2000). Kinetic, thermodynamic, and developmental consequences of deleting creatine kinase isoenzymes from the heart: Reaction kinetics of the creatine kinase isoenzymes in the intact heart. J. Biol. Chem., 275(26), 19742-19746.

O'Brien, S.E., Apkon, M., Berul, C.I., Patel, H.T., Saupe, K., Spindler, M., Ingwall, J.S., & Zahler, R. (2000). Phenotypical features of long Q-T syndrome in transgenic mice expressing human Na-K-ATPase α₃-isoform in hearts. Am. J. Physiol. Heart Circ. Physiol., 279, H2133-H2142.

Saupe, K. W., Eberli, F. R., Ingwall, J. S., & Apstein, C.S. (1999). Hypoperfusion-induced contractile failure does not require changes in cardiac energetics. Am. J. Physiol., Heart and Circ. Physiol, 276, H1715-H1723.

Spindler, M., Saupe, K.W., Tian, R., Ahmed, S., Matlib, M.A., & Ingwall, J.S. (1999). Altered creatine kinase enzyme kinetics in diabetic cardiomyopathy. A 31P NMR magnetization transfer study of the intact beating rat heart. J. Mol. Cell. Cardiol., 31(12), 2175-2189.

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