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670 W. Baltimore Street Baltimore, MD 21201

Phone (Primary):

(410) 706-1646


(410) 706-1622

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Education and Training

Highlighted Publications

  1. Leitch, C.C., Lodh, S., Prieto-Echague, V., Badano, J.L., Zaghloul, N.A. (2014) "Basal body proteins regulate Notch signaling via endosomal trafficking." Journal of Cell Science, Jun 1;127(Pt 11):2407-19.
  2. O'Hare, E.A., Wang, X., Montasser, M.E., Chang, Y.C., Mitchell, B.D., Zaghloul, N.A. (2014) "Disruption of ldlr causes increased LDL-cholesterol and vascular lipid accumulation in a zebrafish model of hypercholesterolemia." Journal of Lipid Research, 55(11): 2242-53.
  3. Lodh, S., Hostelly, T.L., Leitch, C.C., O’Hare, E.A., Zaghloul, N.A. (2015) "Differential effects on ß-cell mass by disruption of Bardet-Biedl Syndrome and Alsrom Syndrome genes." Human Molecular Genetics, 25(1): 57-68. Epub 2015 Oct 22.
  4. O'Hare, E.A., Yerges-Armstrong, L., Perry, J.A., Shuldiner, A.R., Zaghloul, N.A. (2016) "Assignment of functional relevance to genes at type 2 diabetes-associated loci through investigation of ß-cell mass deficits." Molecular Endocrinology, 30(4): 429-445.
  5. Hostelley, T.L., Lodh, S., Zaghloul, N.A. (2016) "Whole organism transcriptome analysis of zebrafish models of Bardet-Biedl Syndrome and Alstom Syndrome provides mechanistic insight into shared and divergenet phenotypes." BMC Genomics, 2016, 17:318.
  6. O'Hare, E.A., Yang, R., Yerges-Armstrong, L., Sreenivasan, U., McFarland, R., Leitch, C.C., Wilson, M.H., Narina, S., Gorden, A., Ryan, K., Shuldiner, A.R., Farber, S.A., Wood, G.C., Still, C.D., Gerhard, G.S., Robishaw, J.D., Sztalryd, C., Zaghloul, N.A. (2017) "TM6SF2 rs58542926 impacts lipid processing in liver and small intestine." Hepatology, Epub ahead of print.
  7. Montasser, M.E., O’Hare, E.A., Wang, X., Howard, A.D., McFarland, R., Perry, J.A., Ryan, K.A., Rice, K., Jaquish, C.E., Shuldiner, A.R., Miller, M., *Mitchell, B.D., *Zaghloul, N.A., *Chang, Y.C. (2018) “An APOO pseudogene on chromosome 5q is associated with LDL-C levels.” Circulation, 138(13):1343-1355.
  8. Nesmith,J.E., Hostelley, T.L., Leitch, C.C., Matern, M.S., Sethna, S., McFarland, R.,Lodh,S., Westlake, C.J., Hertzano, R., Ahmed, Z.M., Zaghloul,N.A. (2019) "Genomic knockout of alms1 in zebrafish recapitulates Alström syndrome and provides insight into metabolic phenotypes." Human Molecular Genetics, In Press.



Additional Publication Citations

A full list of publications can be found at:

Research Interests

Our research focuses on understanding the function of genes that cause complex metabolic phenotypes, such as diabetes and obesity. To investigate this problem, we are pursuing two lines of questioning:

  1. Functional assessment of genes associated with common, complex disorders: Using the zebrafish system and cell models, we are investigating how common variants in disease-associated genes produce metabolic phenotypes. We use targeted disruption of gene expression in zebrafish embryos or cultured cell lines as well as addition of environmental factors, such as high fat diet, to understand what aspects of disease are regulated by susceptibility genes. Our goal is to understand how genetic variants contribute to disease risk and how that contribution is exacerbated in the presence of environmental triggers.
  2. Investigation of rare disorders characterized by obesity and other related features: Disorders that are caused by defects in primary cilia (ciliopathies) display obesity and other metabolic syndrome defects. To understand this, we are investigating how ciliopathy genes contribute to developmental defects in organ systems – such as pancreas and hypothalamus - that might underlie obesity and diabetes. By focusing on such defects in the context of ciliopathies, we hope to understand the pathways that contribute to these phenotypes and shed light onto other more common diseases with similar features.
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