Mulvihill, Erin

Overview 

Erin E Mulvihill, PhD is a Scientist and Director of the Vascular and Metabolic Disease Research Laboratory at the University of Ottawa Heart Institute; and an Assistant Professor, Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, at the University of Ottawa.

Background 

Dr. Erin Mulvihill obtained her PhD in Biochemistry from the University of Western Ontario under the supervision of Murray Huff, PhD in the Vascular Biology Group at the Robarts Institute. During her doctoral studies, Dr Mulvihill’s work focused on understanding how interventions with pharmacotherapy and naturally-occurring flavonoid compounds can target hepatic lipoprotein production and prevent the formation of atherosclerotic lesions. 

Dr. Mulvihill completed postdoctoral training under the supervision of Dr. Daniel Drucker, a notable leader in the fields of incretin biology and Type 2 Diabetes at the Lunenfeld-Tanenbaum Research Institute, located at Mount Sinai Hospital. During her postdoctoral tenure, Dr Mulvihill led a detailed molecular assessment of how DPP4 inhibitors lower blood glucose, using a combination of mouse genetics and pharmacology. She has also been involved in understanding how incretin therapies impact cardiovascular disease using a number of experimental mouse models.Dr. Mulvihill joined the University of Ottawa and University of Ottawa Heart Institute in July 2017. 

Dr Mulvihill currently holds an Early Career Investigator NSERC Discovery Grant, and was a recipient of a Lunenfeld-Tanenbaum Research Institute Innovation Grant in 2016.

Research & Clinical Interests 

Dr Mulvihill’s expertise in lipids and lipoproteins, models of diabetes and cardiovascular disease, intestinal biology and mouse genetics, her research program contributes to improving our understanding of the molecular events which contribute to metabolic and cardiovascular disease.

Publications 

See current publications list at PubMed.

Selected publications:

1. Cellular Sites and Mechanisms Linking Reduction of Dipeptidyl Peptidase-4 Activity to Control of Incretin Hormone Action and Glucose Homeostasis. Mulvihill EE, Varin EM, Gladanac B, Campbell JE, Ussher JR, Baggio LL, Yusta B, Ayala J, Burmeister MA, Matthews D, Bang KW, Ayala JE, Drucker DJ. 
Cell Metab. 2017;10;25(1):152-165.

2. Inhibition of Dipeptidyl Peptidase-4 Impairs Ventricular Function and Promotes Cardiac Fibrosis in High Fat-Fed Diabetic Mice. Mulvihill EE, Varin EM, Ussher JR, Campbell JE, Bang KW, Abdullah T, Baggio LL, Drucker DJ. Diabetes. 2016;65(3):742-54.

3. TCF1 links GIPR signaling to the control of beta cell function and survival. Campbell JE, Ussher JR, Mulvihill EE, Kolic J, Baggio LL, Cao X, Liu Y, Lamont BJ, Morii T, Streutker CJ, Tamarina N, Philipson LH, Wrana JL, MacDonald PE, Drucker DJ. Nat Med. 2016;22(1):84-90.

4. Naringenin prevents obesity, hepatic steatosis, and glucose intolerance in male mice independent of fibroblast growth factor 21.Assini JM, Mulvihill EE, Burke AC, Sutherland BG, Telford DE, Chhoker SS, Sawyez CG, Drangova M, Adams AC, Kharitonenkov A, Pin CL, Huff MW. Endocrinology. 2015;156(6):2087-102.

5. Inactivation of the cardiomyocyte glucagon-like peptide-1 receptor (GLP-1R) unmasks cardiomyocyte-independent GLP-1R-mediated cardioprotection. Ussher JR, Baggio LL, Campbell JE, Mulvihill EE, Kim M, Kabir MG, Cao X, Baranek BM, Stoffers DA, Seeley RJ, Drucker DJ. Mol Metab. 2014;9;3(5):507-17.

6. Naringenin prevents cholesterol-induced systemic inflammation, metabolic dysregulation, and atherosclerosis in Ldlr⁻/⁻ mice. Assini JM, Mulvihill EE, Sutherland BG, Telford DE, Sawyez CG, Felder SL, Chhoker S, Edwards JY, Gros R, Huff MW. J Lipid Res. 2013;54(3):711-24.

7. GLP-1 receptor activation indirectly reduces hepatic lipid accumulation but does not attenuate development of atherosclerosis in diabetic male ApoE(-/-) mice. Panjwani N, Mulvihill EE, Longuet C, Yusta B, Campbell JE, Brown TJ, Streutker C, Holland D, Cao X, Baggio LL, Drucker DJ. Endocrinology. 2013;154(1):127-39.

8. Nobiletin attenuates VLDL overproduction, dyslipidemia, and atherosclerosis in mice with diet-induced insulin resistance. Mulvihill EE, Assini JM, Lee JK, Allister EM, Sutherland BG, Koppes JB, Sawyez CG, Edwards JY, Telford DE, Charbonneau A, St-Pierre P, Marette A, Huff MW. Diabetes. 2011;60(5):1446-57.

9. Naringenin decreases progression of atherosclerosis by improving dyslipidemia in high-fat-fed low-density lipoprotein receptor-null mice. Mulvihill EE, Assini JM, Sutherland BG, DiMattia AS, Khami M, Koppes JB, Sawyez CG, Whitman SC, Huff MW. Arterioscler Thromb Vasc Biol. 2010;30(4):742-8.

10. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDL receptor-null mice with diet-induced insulin resistance. Mulvihill EE, Allister EM, Sutherland BG, Telford DE, Sawyez CG, Edwards JY, Markle JM, Hegele RA, Huff MW. Diabetes. 2009;58(10):2198-210.

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