Back to Main

Faculty Detail    
Name ADAM R WENDE
Assistant Professor
 
Campus Address VH G019 Zip 0019
Phone 205-975-6272
E-mail arwende@uab.edu
Other websites Google Scholar
PubMed
     

Education
Undergraduate  Knox College    2000  BA in Biochemistry and Biology 
Graduate  Washington University in St. Louis    2006  PhD in Molecular Cellular Biology 
Fellowship  University of Utah    2013  Postdoctoral studies 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Assistant Professor
Secondary  Biomedical Engineering  Biomedical Engineering Assistant Professor
Center  Comprehensive Cardiovascular Ctr  Comprehensive Cardiovascular Ctr Assistant Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Assistant Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Assistant Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cell, Molecular, & Developmental Biology 
Genetics and Genomic Sciences 
Molecular and Cellular Pathology Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr. Wende has spent the last decade exploring the regulation of glucose utilization in heart and muscle. After completing his undergraduate biochemistry degree and an Honors Thesis with Dr. Mark R. Brodl at Knox College in Galesburg, IL he went on to undertake his Ph.D. training in the Cardiology Department at Washington University in St. Louis, MO studying transcriptional regulation with Dr. Daniel P. Kelly. He then joined the University of Utah in 2006 to pursue his postdoctoral studies with Dr. E. Dale Abel examining upstream regulation by cellular signaling and the resulting changes in mitochondrial physiology. Then in August of 2013, he joined the faculty at The University of Alabama at Birmingham in the Division of Molecular and Cellular Pathology as an Assistant Professor.

His work has been funded by the American Heart Association, the JDRF, and most recently by an NIH K99/R00 award. With these training experiences he has expanded his research through use of transgenic and diabetes mouse models to identify molecular and genetic mechanisms of glucose-mediated control of mitochondrial function. His outside interests include time with his wife and two young daughters and running marathons.

Society Memberships
Organization Name Position Held Org Link
American Diabetes Association  Member  ADA 
American Heart Association  Member  AHA 
American Physiological Society  Member  APS 

Research/Clinical Interest
Title
Mechanisms of glucose mediated regulation of cardiac mitochondrial function
Description
Work in the laboratory has two primary goals: 1) to determine the role of metabolic substrate switching in the hearts of individuals with diabetes or heart failure, and 2) to define the role of cellular glucose delivery on post-translational regulation of mitochondrial enzyme activity and epigenetic regulation of gene expression that together may lead to the development of diabetic cardiomyopathy. The primary goal of the R00 funded research is to determine the role the protein post-translational modification O-GlcNAc has in regulating cardiac cellular function and define the role that changes in glucose levels have on long-lasting epigenetic regulation of gene expression in a process termed “glycemic memory”. By defining these molecular signatures of altered protein regulation and DNA structure/regulation we aim to provide critical knowledge to determining future therapeutic interventions for diabetic and heart failure patients.

Selected Publications 
Publication PUBMEDID
Young ME, Brewer RA, Peliciari-Garcia RA, Collins HE, He L, Birky TL, Peden BW, Thompson EG, Ammons BJ, Bray MS, Chatham JC, Wende AR, Yang Q, Chow CW, Martino TA and Gamble KL. Cardiomyocyte-specific BMAL1 plays critical roles in metabolism, signaling, and maintenance of contractile function of the heart. Journal of Biological Rhythms, 29(4):257-276, 2014.  25238855 
Riehle C, Wende AR, Zhu Y, Oliveira KJ, Pereira RO, Jaishy BP, Bevins J, Valdez S, Noh J, Kim BJ, Moreira AB, Weatherford ET, Manivel R, Rawlings TA, Rech M, White MF and Abel ED. Insulin receptor substrates (IRS) are essential for the bioenergetic and hypertrophic response of the heart to exercise training. Molecular and Cellular Biology, 34(18):3450-3460, 2014.  25002528 
Pereira RO, Wende AR, Crum A, Hunter D, Olsen CD, Rawlings T, Riehle C, Ward WF and Abel ED. Maintaining PGC-1alpha; expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function. The FASEB Journal, 28(8):3691-3702, 2014.  24776744 
Addison O, Drummond MJ, LaStayo PC, Dibble LE, Wende AR, McClain DA and Marcus RL. Intramuscular fat and inflammation differ in older adults: The impact of frailty and inactivity. The Journal of Nutrition, Health and Aging, 18(5):532-538, 2014.  24886741 
Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Riehle C and Abel ED. GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure. Journal of Molecular and Cellular Cardiology, 72:95-103, 2014.  24583251 
Lopez-Izquierdo A, Pereira RO, Wende AR, Punske BB, Abel ED and Tristani-Firouzi M. The absence of insulin signaling in the heart induces changes in potassium channel expression and ventricular repolarization. American Journal of Physiology – Heart and Circulatory Physiology, 306(5):H747-754, 2014.  24375641 
Riehle C, Wende AR, Sena S, Pires KM, Pereira RO, Zhu Y, Bugger H, Frank D, Bevins J, Chen D, Perry CN, Dong XC, Valdez S, Sheng X, Weimer BC, Gottlieb RA, White MF and Abel ED. Insulin receptor substrates are required for suppressing neonatal autophagy in the heart. The Journal of Clinical Investigation, 123(12):5319-5333, 2013.  24177427 
Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Anderson SM and Abel ED. Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction. Journal of the American Heart Association, 2(5):e000301, 2013.  24052497 
Wende AR and Young ME. APpEaLINg therapeutic target for obesity cardiomyopathy? Journal of Molecular and Cellular Cardiology, 63:165-168, 2013.  23948484 
Zhu Y, Soto J, Anderson B, Riehle C, Zhang YC, Wende AR, Jones D, McClain DA and Abel ED. Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1alpha. American Journal of Physiology - Heart and Circulatory Physiology, 305(1):H41-51, 2013.  23624629 
Shibayama J, Taylor TG, Venable PW, Rhodes NL, Gil R, Warren M, Wende AR, Abel ED, Cox J, Spitzer KW and Zaitsev AV. Metabolic determinants of electrical failure in ex vivo canine model of cardiac arrest: Evidence for the protective role of inorganic pyrophosphate. PLoS One, 8(3):e57821, 2013.  23520482 
Zhu Y, Pereira RO, O’Neill BT, Riehle C, Ilkun O, Wende AR, Rawlings TA, Zhang YC, Zhang Q, Klip A, Shiojima I, Walsh K and Abel ED. Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation. Molecular Endocrinology, 27(1):172-184, 2013.  23204326 
Sohn K, Wende AR, Abel ED, Moreno AP, Sachse F and Punske BB. Absence of glucose transporter 4 diminishes electrical activity of mouse hearts during hypoxia. Experimental Physiology, 98(3):746-757, 2013.  23180812 
Wende AR*, Symons JD* and ED Abel. Mechanisms of Lipotoxicity in the Cardiovascular System. Current Hypertension Reports, 14(6):517-531, 2012.  23054891 
Marcus RL, Addison O, LaStayo PC, Hungerford R, Wende AR, Hoffman JM, Abel ED and McClain DA. Regional muscle glucose uptake remains elevated 1 week after cessation of resistance training independent of altered insulin sensitivity response in older adults with type 2 diabetes. The Journal of Endocrinological Investigation, 98(3):746-757, 2013.  22522495 
Bugger H, Riehle C, Jaishy, Wende AR, Tuinei J, Chen D, Soto J, Pires KM, Boudina S, Theobald HA, Luptak I, Wayment B, Wang X, Litwin SE, Weimer BC and Abel ED. Genetic loss of insulin receptors worsens cardiac efficiency in diabetes. Journal of Molecular and Cellular Cardiology, 52(5):1019-1026, 2012.  22342406 
Li Y, Wende AR, Nunthakungwan O, Huang Y, Hu E, Jin H, Boudina S, Abel ED and Jalili T. Cytosolic, but not mitochondrial, oxidative stress likely contributes to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice. The FEBS Journal, 279(4):599-611, 2012.  22221582 
Sohn K, Sachse FB, Moreno AP, Ershler PR, Wende AR, Abel ED and Punske BB. The maximal downstroke of epicardial potentials as an index of electrical activity in mouse hearts. Transactions on Biomedical Engineering, 58(11):3175-3183, 2011.  21859611 
Riehle C*, Wende AR*, Zaha VG, Pires KM, Wayment B, Olsen C, Bugger H, Buchanan J, Wang X, Moura AB, Doenst T, Medina-Gomez G, Litwin SE, Lelliott CJ, Vidal-Puig A and Abel ED. PGC-1alpha deficiency accelerates the transition to heart failure in pressure overload hypertrophy. Circulation Research, 109(7):783-793, 2011.  21799152 
Pound KM, Arteaga GM, Fasano M, Wilder T, Fischer SK, Warren CM, Wende AR, Farjah M, Abel ED, Solaro RJ and Lewandowski ED. Expression of slow skeletal TnI in adult mouse hearts confers metabolic protection to ischemia. Journal of Molecular and Cellular Cardiology, 51(2):236-234, 2011.  21640727 
Symons JD, Hu P, Yang Y, Wang X, Zhang Q, Wende AR, Sloan CL, Sena S, Abel ED and Litwin S. Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload. American Journal of Physiology – Heart and Circulatory Physiology, 300(1):H374-381, 2011.  20971769 
O'Grady SP, Wende AR, Remien CH, Valenzuela LO, Enright LE, Chesson LA, Abel ED, Cerling TE and Ehleringer JR. Aberrant water homeostasis detected by stable isotope analysis. PLoS One, 5(7):e11699, 2010.  20657736 
Banke NH, Wende AR, Leone TC, O'Donnell JM, Abel ED, Kelly DP, Lewandowski ED. Preferential oxidation of triacylglyceride-derived fatty acids in heart is augmented by the nuclear receptor PPARα. Circulation Research, 107(2):233-241, 2010.  20522803 
Wende AR, Soto J, Olsen CD, Pires KM, Schell JC, Larrieu-Lahargue F, Litwin SE, Kakoki M, Takahashi N, Smithies O and Abel ED. Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic Akita mice. Endocrinology, 151(8):3536-3542, 2010.  20501666 
Wende AR and Abel ED. Lipotoxicity in the heart. Biochimica et Biophysica Acta, 1801(3):311-319, 2010.  19818871 
Kim J, Wende AR, Sena S, Theobald HA, Soto J, Sloan C, Wayment BE, Litwin SE, Holzenberger M, LeRoith D and Abel ED. Insulin-like growth factor-1 (IGF-1) receptor signaling is required for exercise-induced cardiac hypertrophy. Molecular Endocrinology, 22(11):2531-2543, 2008.  18801929 
Wende AR, Schaeffer PJ, Parker GL, Zechner C, Han DH, Chen MM, Hancock CR, Lehman JJ, Huss JH, McClain DA, Holloszy JO and Kelly DP. A role for the transcriptional coactivator PGC-1alpha in muscle refueling. The Journal of Biological Chemistry, 282(50):36642-36651, 2007.  17932032 
O’Neill BT, Kim J, Wende AR, Theobald HA, Tuinei J, Buchanan J, Guo A, Zaha VG, Davis DK, Schell JC, Boudina S, Wayment B, Litwin SE, Shioi T, Izumo S, Birnbaum MJ and Abel ED. A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy. Cell Metabolism, 6(4):294-306, 2007.  17908558 
Sena S*, Rasmussen IR*, Wende AR, McQueen AP, Theobald HA, Wilde N, Pereira RO, Litwin SE, Berger JP and Abel ED. Cardiac hypertrophy caused by peroxisome proliferator-activated receptor-gamma agonist treatment occurs independently of changes in myocardial insulin signaling. Endocrinology, 148(12):6047-6053, 2007.  17823261 
Burgess SC, Leone TC, Wende AR, Croce MA, Chen Z, Sherry AD, Molloy CR and Finck BN. Diminished hepatic gluconeogenesis via defects in TCA cycle flux in PPARgamma coactivator-1alpha (PGC-1alpha)-deficient mice. The Journal of Biological Chemistry, 281(28):19000-19008, 2006.  16670093 
Wende AR, Huss JM, Schaeffer PJ, Giguère V and Kelly DP. PGC-1alpha coactivates PDK4 gene expression via the orphan nuclear receptor ERRalpha: A mechanism for transcriptional control of muscle glucose metabolism. Molecular and Cellular Biology, 25(24):10684-10694, 2005.  16314495 
Leone TC, Lehman JL, Finck BN, Schaeffer PJ, Wende AR, Boudina S, Courtois M, Wozniak DF, Sambandam N, Bernal-Mizrachi C, Chen Z, Holloszy JO, Medeiros DM, Schmidt RE, Saffitz JE, Abel ED, Semenkovich CF and Kelly DP. PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis. PLoS Biology, 3(4):e101, 2005.  15760270 
Schaeffer PJ, Wende AR, Magee CJ, Neilson JR, Leone TC, Chen F and Kelly DP. Calcineurin and CaM kinase signaling pathways activate distinct metabolic gene regulatory programs in cardiac muscle: evidence for activation of PPARalpha by calcineurin. The Journal of Biological Chemistry, 279(38):39593-39603, 2004.  15262994 
Baar K, Wende AR, Jones TE, Marison M, Nolte LA, Chen M, Kelly DP and Holloszy JO. Adaptations of muscle to exercise: rapid increase in the transcriptional coactivator PGC-1. The FASEB Journal, 16(14):1879-1886, 2002.  12468452 

Keywords
Diabetes, Hypertension, Exercise, Mitochondria, Metabolism, Glucose, Epigenetics, Gene expression, transcription, O-GlcNAc, protein modifications, DNA methylation, Histone modification, GLUT4, PDK2, PDK4