> Dr May Faraj |
Contact info
Dr May Faraj
Clinical Research Institute of Montreal (IRCM)
110, Pins Avenue West - Office 1770.2
Montr�al, QC H2W 1R7
Tel: 1-514-987-5655
Fax: 1-514-987-5645
E-mail: [email protected]
Research keywords
- Human nutrition
- Lipoproteins
- Adipose tissue
- Inflammation
- Insulin secretion
- Insulin sensitivity
- Metabolic disease
- Type 2 diabetes
- Obesity
- Stable isotopes
- Post-menopausal women
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May Faraj, PDt, PhD
Associate professor of research, Department of Nutrition
Biographical Sketch
May Faraj obtained her MSc in Nutrition and her PhD in Experimental
medicine from McGill University in Montreal under the supervision of Dr Katherine
Cianflone. Her graduate work investigated the regulation of lipoprotein lipase activity,
lipoprotein metabolism and fatty acid trapping in adipose tissue using cell, mice and
human models. In 2004, she joined the lab of Dr Remi Rabasa-Lhoret, Department of
Nutrition, University of Montreal, as a CIHR-postdoctoral fellow exploring insulin
action and sensitivity in humans. In 2007 she obtained CIHR New Investigator Award and
an academic position as an assistant professor/junior scientist in the Department of
Nutrition, University of Montreal. She then joined Clinical Research Institute of Montreal
(IRCM) in 2008 as an invited scientist, where she started her clinical research lab funded
by CIHR operating grants and CFI leader's opportunity funds and in collaboration with Dr
Rabasa-Lhoret and IRCM physicians. Most recently in 2013, she was awarded FRSQ salary support,
Chercheure boursi�re � Junior 2, in Clinical and epidemiological research. Her research
explores a hypothesis she instigated in 2006 linking the number of apoB-lipoproteins to the
promotion and prevention of type 2 diabetes in humans. She is a member of L'Ordre
Professionnel des Di�t�tistes du Qu�bec since 1999.
Click here for PubMed listing
Research Interests
The research of Dr Faraj focuses on investigating the hypothesis that elevated
numbers of atherogenic or apoB-lipoproteins (measured as plasma apoB) may be a cause and not only
a consequence of type 2 diabetes in humans. She examines whether apoB-lipoproteins may activate
mechanisms that are known to promote type 2 diabetes in humans, and particularly in obesity,
namely inflammation, dysfunctional adipose tissue, hyperinsulinemia and insulin resistance.
Moreover, she investigates whether targeting subjects with the hyperapoB phenotype (i.e.
elevated plasma apoB) by nutritional interventions may reduce plasma apoB and associated
cardiometabolic risks in these subjects. To investigate these hypotheses, she utilizes
complementary in vivo, ex vivo (adipose tissue) and in vitro (adipocytes
and macrophage) techniques to follow the metabolism of dietary fat (stable and radioactive isotopes
studies), to assess inflammation (cytokine secretion, immunohistochemistry and gene expression), to
fractionate and characterize lipoproteins (ultracentrifugation, FPLC, gel electrophoresis) and to
assess insulin secretion, sensitivity and action (Botnia clamp and insulin-induced glucose/lipid
cellular metabolism).
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