Jessica Ellis

Educational Background

  • B.S. , Science of Nutrition at Virgina Tech in 2003
  • Post-Bac, NIH-NIDDK Genetics of Development and Disease Branch at in 2005
  • Ph.D., Nutritional Biochemistry at University of North Carolina at Chapel Hill in 2010
  • Post-Doc, Biological Chemistry at Johns Hopkins University in 2014

Activities & Memberships

  • American Society for Cell Biology (ACB), 2013 - Present
  • American Society for Biochemistry and Molecular Biology (ASBMB), 2008 - Present
  • American Society of Nutrition (ASN), 2006 - Present


Abnormally high levels of fat metabolism, particularly in the muscle, play a key role in the development of diabetes and diabetes-related heart disease. The lab aims to target the breakdown of fats in the muscle and heart to prevent and improve diabetes and related complications. These goals will be accomplished using novel conditional genetic animal models combined with dietary and exercise paradigms, as well as biochemical and molecular techniques. The long-term goal of this work is to provide mechanistic insight into the metabolic underpinnings of diabetes and ultimately shape therapeutic strategies aimed at reversing insulin resistance and preventing diabetes-related mortality.

Aberrations in fatty acid metabolism impair neurological function and influence disparate neurodegenerative and neuropsychiatric diseases. Furthermore, dietary lipids influence the development and progression of many neurological disorders, yet the mechanisms that control the metabolism of dietary fatty acids within the brain remain unclear. The long-term goal of this work is to understand how the regulatory mechanisms that control fatty acid metabolism within the brain protect neurons from oxidative damage. The lab focuses on enzymes that control the formation and retention of acyl-CoAs, acyl-CoAs are the activated form of fatty acids whose synthesis is required for downstream metabolism, and for cellular fatty acid retention. The lab employs the use of recombinant enzymes, knockout/transgenic mouse models and cell culture to understand enzymes that control acyl-CoA metabolism. This work will elucidate the control of brain fatty acid metabolism and have broad-reaching impact on therapeutic and preventative measures for neurological health and disease.

Discovery Publications

  • Damen, F., Berman, A., Soeprinatrna, A., Ellis, J.M., Buttars, S., Aasa, K., Goergen, C.J. (2017) High Frequency Four-Dimensional Ultrasound (4DUS): A Reliable Method for Assessing Murine Cardiac Function. Tomography. 292(45):18443-18456. PMID: 28916721.
  • Pereyra, A.P., Hasek, L.Y., Harris, K.L., Berman, A.G., Damen, F.W., Goergen, C.J., Ellis, J.M. (2017) Loss of cardiac carnitine palmitoyltransferase 2 results in rapamycin-resistant, acetylation-independent hypertrophy.  J. Biol Chem. 292 (45):18443-18456. PMID: 28916721.
  • Wall, V.Z., Barnhart, S., Kramer, F., Kanter, J.E., Vivekanandan-Giri, A., Pennathur, S., Bolego, C., Ellis, J.M., Gijón, M.A., Wolfgang, M.J., Bornfeldt, K.E. (2017) Inflammatory Stimuli Induce Acyl-CoA Thioesterase 7 and Remodeling of Phospholipids Containing Unsaturated Long (≥C20)-Acyl Chains in Macrophages. J Lipid Res. 8(6):1174-1185. PMID: 28416579.
  • Grevengoed, T.J., Cooper, D.E., Young, P.A., Ellis, J.M., Coleman, R.A. (2015) Loss of long-chain acyl-CoA synthetase isoform 1 impairs cardiac autophagy and mitochondrial structure through mechanistic target of rapamycin complex 1 activation. FASEB J. 29(11):4641-53. PMID: 26220174.
  • Schisler, J.C., Grevengoed, T.J., Pascual, F., Cooper, D.E., Ellis, J.M., Paul, D.S., Willis, M.S., Patterson, C., Jia, W., Coleman, R.A. (2015) Cardiac energy dependence on glucose increases metabolites related to glutathione and activates metabolic genes controlled by mTOR. J Am Heart Assoc. 29(11):4641-53. PMID: 26220174.
  • Frey, J.L., Li, Z., Ellis, J.M., Zhang, Q., Farber, C.R., Aja, S., Wolfgang, M.J., Clemens, T.L., Riddle, R.C. (2015) Wnt-Lrp5 signaling regulates fatty acid metabolism in the osteoblast. Mol Cell Biol. 35(11):1979-91. PMID: 25802278.
  • Ellis, J.M., Bowman, C.E., Wolfgang, M.J. (2015) Metabolic and tissue-specific regulation of acyl-CoA metabolism.  PLoS One. 10(3):e0116587. PMID: 25760036.
  • Lee, J., Ellis, J.M., Wolfgang, M.J. (2015) Adipose fatty acid oxidation is required for thermogenesis and potentiates oxidative stress induced inflammation. Cell Rep. 10(2):266-79. PMID: 25578732.
  • Paul, D.S., Grevengoed, T.J., Pascual, F., Ellis, J.M., Willis, M.S., Coleman, R.A.  (2014) Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin. Biochim Biophys Acta. 1841(6):880-7. PMID: 24631848.
  • Rodriguez, S., Ellis, J.M., Wolfgang, M.J. (2014) Chemical-genetic induction of Malonyl-CoA decarboxylase in skeletal muscle. BMC Biochem 15(1):20. PMID: 25152047.
  • Ellis, J.M., Wong, G.W., & Wolfgang, M.J.  (2013) Acyl Coenzyme A Thioesterase 7 regulates neuronal fatty acid metabolism to prevent neurotoxicity. Mol Cell Biol. 33(9):1869-1882. PMID: 23459938.
  • Ellis, J.M. & Wolfgang, M.J. (2012) A genetically encoded metabolite sensor for malonyl-CoA.  Chem Biol. 19(10):1333-1339. PMID: 23102226.
  • Teng, Y.W., Ellis, J.M., Coleman, R.A., & Zeisel, S.H. (2012) Mouse betaine-homocysteine S-Methyltransferase deficiency reduces body fat via increasing energy expenditure and impairing lipid synthesis and enhancing glucose oxidation in white adipose tissue. J Biol Chem. 287(20):16187-98. PMID: 22362777.
  • Watkins, P.A. & Ellis, J.M. (2012) Peroxisomal acyl-CoA synthetases. Biochim Biophys Acta. 1822(9):1411-20. PMID: 22366061. 
  • Ellis, J.M., Paul, D.S., DePetrillo, M.A., Singh, B.P., Malarkey, D.E., Coleman, R.A. (2012) Mice deficient in glycerol-3-phosphate acyltransferase-1 have a reduced susceptibility to liver cancer. Toxicol Pathol. 40(3):513-21. PMID: 22215515. 
  • Ellis, J.M., Mentock, S.M., DePetrillo, M.A., Koves, T.R., Sen, S., Watkins, S.M., Muoio, D.M., Cline, G.W., Taegtmeyer, H., Shulman, G.I., Willis, M.S., Coleman, R.A. (2011) Mouse cardiac Acyl Coenzyme A synthetase 1 deficiency impairs fatty acid oxidation and induces cardiac hypertrophy. Mol Cell Biol. 31(6):1252-62. PMID: 21245374. 
  • Ellis, J.M., Li. L.O., Wu, P.C., Koves, T.R., Stevens, R.D., Watkins, S.M., Muoio, D.M., Coleman, R.A. (2010) Adipose acyl-CoA synthetase-1 (ACSL1) directs fatty acids towards β-oxidation and is required for cold thermogenesis. Cell Metab. 12(1):53-64. PMID: 20620995. 
  • Ellis, J.M., Frahm, J.L., Li, L.O., Coleman, R.A. (2010) Acyl-CoA synthetases in metabolic control. Curr Opin Lipidol. 21(3):212-17. PMID: 20480548. 
  • Li, L.O., Ellis, J.M., Paich, H.A., Wang, S., Gong, N., Altshuller, G.N., Thresher, R.J., Koves, T.R., Watkins, S.M., Muoio, D.M., Cline, G.W., Shulman, G.I., Coleman, R.A. (2009) Liver-specific loss of long-chain acyl-CoA synthetase-1 decreases triacylglycerol synthesis and beta-oxidation, and alters phospholipid fatty acid composition. J. Biol Chem. 284(41):27816-26. PMID: 19648649.
  • Kono, M., Dreier, J.L., Ellie, J.M., Allende, M.L., Kalkofen, D.N., Sanders, K.M., Bielawski, J., Bielawaska, A., Hannun, Y.A., Proia, R.L. (2006) Neutral ceramidase encoded by the Asah2 gene is essential for the intestinal degradation of sphingolipids. J Biol Chem. 281(11):7324-31. PMID: 16380386. 
  • Yamashita, T., Wu, Y.P., Sandhoff, R., Geyer, R., Werth, N., Ellis, J.M., Dupree, J., Sandhoff, K., Proia, R. (2005) Interruption of ganglioside synthesis produces central nervous system degeneration and altered axon-glial interactions. Proc Natl Acad Sci USA. 102(8):2725-30. PMID: 15710896. 


NUTR 43700 Macronutrient Metabolism in Health and Disease
NUTR 59000 Lipid Regulation and Cell Function
NUTR TBA Nutrition Science Research and Translation in Health and Disease

Jessica Ellis

Assistant Professor

Office: STON 206
Phone: 765-496-0142
Fax: 765-494-0674
Lab Website

Department of Nutrition Science, 700 W. State Street, West Lafayette, IN 47907-2059(765) 494-8228, Fax: (765) 494-0674

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