My research interests are focused on understanding the molecular mechanisms implicated in the development and the rescue of Non-Alcoholic Fatty Liver Disease (NAFLD). For many years, I have been investigating the different pathways involved in the development of the disease including fat absorption by the intestine, cellular fatty acid uptake, the oxidation of fat in the mitochondria as well as the assembly and secretion of fat into lipoproteins in the blood. I use both genetic and dietary interventions mouse models for NAFLD. I have extensive expertise in metabolic studies both in vivo as well as in vitro using immortalized cell lines as well as primary isolated cells (hepatocytes, enterocytes). The goal is to translate the findings in animal and cell models to humans where obesity and excess nutrients causes cellular stress and metabolic diseases including NAFLD, insulin resistance and diabetes. I believe that an integrated understanding of these pathways will lead to the identification of novel therapeutic targets for the disease.
Currently, Dr. Nassir is investigating sirtuins as modulators of these different metabolic pathways in the liver and as novel therapeutic targets for NAFLD.
Areas of Expertise
- Mitochondria in nonalcoholic liver diseases
- Sirtuins and NAFLD
- Lipid and lipoprotein metabolism as it relates to obesity diabetes and Non-alcoholic Fatty liver disease
- Inflammation as it relates to Non-alcoholic Fatty liver disease
- Fatty acid transport: Role of CD36 in hepatic and intestinal lipid metabolism and in inflammation
- Nutritional status in minerals and oligo-elements in the regulation of hepatic lipid metabolism
Education & Training
University Blaise Pascal/Institute of Human Nutrition, France
Awards & Honors
Honors and Awards
- 1990-1991 First prize from the French Association of Nutrition (AFN)
- 1994 Highest Honors: Doctorate, University Blaise Pascal, France
- 1995 Qualification for lecturer in Cellular Biology (Qualification #9526540103, Paris 2/28/1995)
- 1999 Digestive Disease Week: Oral presentation
- 2000 Digestive Disease Week: Poster of distinction.
- 2006 FASEB Travel Award: Summer Research Conference, Molecular Biology of Intestinal Lipid Transport and Metabolism, Tucson Arizona.
- 2015 Digestive Disease Week: Oral presentation
- 2016 American Association of Study of Liver Diseases: Invited lecture, Parallel session
- 2016-present School of Medicine Research council member
- 2016 School of Medicine Mentoring Award sub-committee (Chair)
- 2016-2017 Women in Medicine and Medical Sciences (WIMMS) spring retreat committee
- American Heart Association (AHA), Council on Atherosclerosis, Thrombosis and Vascular Biology
- American Gastrological Association (AGA)
- American Association for the Study of Liver Disease (ASSLD)
- American Association for the Advancement of Science (AAAS)
- European Association for the Study of the Liver (EASL)
- American Journal of Physiology: Gastrointestinal and Liver Physiology
- IEMAMC (Immunology, Endocrine & Metabolic Agents - Medicinal Chemistry)
- PLoS ONE
- Molecular Medicine
- Expert Review of Gastroenterology and Hepatology
- British Journal of Nutrition
- Liver International
- Disease Biomarkers
- BMC Medical genomics
- Abstracts Reviewer- MU SOM-Health Sciences Research Day 11/2016
Peer Reviewed Publications
1. Nassir F, Arndt JJ and Ibdah JA. 2017; SIRT3 Deacetylates Mitochondrial Trifunctional Protein and Rescues NAFLD. (In submission)
2. Nassir F, Arndt JJ, Ibdah, JA. SIRT3 deacetylates the mitochondrial trifunctional protein (MTP) and rescues NAFLD in MTP heterozygous mice. Hepatology, October 2016, 64: S5246.
3. Nassir F, Ibdah JA. Sirtuins and nonalcoholic fatty liver disease. World J Gastroenterol. 2016; 22(46):10084-10092.
4. Nassir F, Rector RS, Hammoud GM, Ibdah JA. Pathogenesis and Prevention of Hepatic Steatosis. Gastroenterol Hepatol. 2015;11(3):167-75.
5. Nassir F, Ibdah JA. Role of Mitochondria in Nonalcoholic Fatty Liver Disease. Int J Mol Sci. 2015; 11(3):167-175.
6. Nassir F, Arndt JJ and Ibdah JA. Hepatic overexpression of SIRT3 in mice heterozygous for mitochondrial trifunctional protein rescues hepatic steatosis and improves insulin sensitivity. Gastroenterology, April 2015, Issue 4, Supplement 1, S-973
7. Nassir F, Ibdah JA. Role of mitochondria in alcoholic liver disease. World J. Gastroenterol. 2014; 20(9):2136-42.
8. Nassir F, Adewole OL, Brunt EM, Abumrad NA. CD36 deletion reduces VLDL secretion, modulates liver prostaglandins, and exacerbates hepatic steatosis in ob/ob mice. J Lipid Res. 2013;54(11):2988-97.
9. Sundaresan S, Shahid, R, Riehl TE, Chandra R, Nassir F, Stenson WF, Liddle RA, Abumrad, NA. CD36-dependent signaling mediates fatty acid induced gut release of secretin and cholecystokinin. FASEB J. 2013; 27(3):1191-02.
1. Book chapter: Abumrad N, Nassir F, Marcus A. Digestion and Absorption of Dietary Fat, Carbohydrate, and Protein. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 10th ed, Feldman M, Friedman LS, Brandt LJ. (Eds), Saunders, Philadelphia 2016. p.17369.
1. Nassir F, Arndt JJ and Ibdah JA. SIRT3 deacetylates the mitochondrial trifunctional protein (MTP) and rescues NAFLD in MTP heterozygous mice. The Boston, MA. Liver Meeting November 11-15, 2016. Parallel session: Steatohepatitis: Experimental II. Lecture presentation.
2. Nassir F, Arndt JJ and Ibdah JA. Hepatic overexpression of SIRT3 in mice heterozygous for mitochondrial trifunctional protein rescues hepatic steatosis and improves insulin sensitivity. Digestive Disease Week, Washington, DC, May 16-19, 2015. Oral presentation.
3. Nassir F, Arndt JJ, Ibdah JA. Hepatic SIRT3 overexpression induces mitophagy and alleviates hepatic steatosis and insulin resistance in mice heterozygous for mitochondrial trifunctional protein. Cell Symposia: Multifaceted Mitochondria. Chicago, July 19-21, 2015.