Dr. Naima Moustaid-Moussa
Postdoc: Molecular Nutrition; Harvard School of Public Health
Ph.D. Endocrinology; University of Paris, France
M.S. Cell Biology and Animal Physiology
Professional Interest: Adipocyte Biology, Endocrinology, Adipokines; The Renin Angiotensin System; Obesity-Diabetes-Insulin resistance-Hypertension; Genomics and Proteomics; Nutrient-Gene Interactions. Animal Models.
Obesity has become an epidemic public health problem worldwide. In the US, nearly a third of adults are obese, and two-thirds are overweight or obese. In addition, the percentage of children and adolescents who are obese has tripled over the past three decades. The medical implications of this epidemic obesity are enormous, especially in the pediatric population, due to increased risk and incidence of diabetes, hypertension, heart disease, certain cancers and premature death in obese individuals, resulting in enormous health case burden.
Human Obesity is a complex disorder, most likely attributed to gene-environmental interactions. Dr. Moustaid-Moussa’s research efforts take advantage of highly relevant animal models for human diseases as well as cell models to understand the cellular and molecular mechanisms underlying obesity. Specifically, her research has focused on a potential role for adipose tissue in triggering and/or potentiating obesity and associated co-morbidity. Indeed, over the past couple of decade, findings from her lab and others have documented an important role for adipose tissue as an endocrine system that impacts not only fat cell expansion but also whole body homeostasis and other distal tissues through the bioactive hormones, metabolites and other substances it secretes into the blood stream. One such hormone of interest to her laboratory is angiotensin II, a hypertensive hormone produced by adipose tissue that her research has shown to promote fat storage in a glucose-dependent and insulin-like manner. The discovery of Angiotensin II in fat cells suggests a potential role of fat cells in obesity-associated hypertension. Her laboratory is using engineered mice models of overexpression or targeted inactivation of angiotensinogen, the hormone precursor, to further dissect this relationship and its modulation by diet, hormones and disease states. In addition to the rodent models for obesity, they are expanding their research to agricultural models as biomedical research tools to dissect the pathogenesis and regulation of human metabolic disorders. One such model they are beginning to study is the swine model with primary interest in the minipig as a model for human nutritional disorders.
Another exciting area she is beginning to explore is that of functional foods. Indeed, the high prevalence of obesity and co-morbid chronic conditions has led to a search for alternative and new nutritional therapies both for prevention and treatment of metabolic disorders. Inflammation is well documented as the basis for obesity-related disorders including cardiovascular disease and diabetes and several bioactive food components have been used to prevent and treat many disease states. Her research program has thus also undertaken an additional approach to identifying mechanisms governing nutrient- gene interactions in obesity including recent interest in understanding how botanicals and dietary supplements impact human health and disease in rodent and swine models.
Dr. Moustaid-Moussa’s laboratory is applying metabolic, genetics, genomics and proteomics applications to better understand the global function of adipocytes and its regulation by nutrients, hormones in obesity, diabetes, and hypertension. They are using both in vitro cultured adipocyte models (primary and cell lines) as well as animal models as described above.
Last but not least, an exiting local resource is the UT Obesity Research Center (http://obesity.tennessee.edu) which provides researchers with multidisciplinary collaborations and thus a great opportunity for students interested in this area for a broad and comprehensive training in both basic and applied obesity research. The UTORC mission is to develop interdisciplinary programs for the prevention and treatment of overweight and obesity that will decrease obesity-related complications, and help people achieve long-term maintenance of a healthy weight.
- Urs, S., Smith, C., Campbell, B., Saxton, A, Taylor, J, Jones Voy, B. and Moustaid-Moussa, N. Gene Expression Profiling in human preadipocytes and adipocytes by microarray. J. Nutr. 134: 762-770,2004.
- Wang, Y., Jones Voy, B., Urs, S., Kim, S., Bejnood, M., Quigley, N., Heo, Y.R., Standridge, M., Andersen, B., Dhar, M., Joshi, M., Wortman, P., Taylor, J.W., Chun, J., Leuze, M., Claycombe, K., Saxton, A.M. & Moustaid-Moussa, N. The human fatty acid synthase gene and de novo lipogenesis are coordinately regulated in human adipose tissue. J. Nutr. 134:1032-1038, 2004.
- Yvan-Charvet L, Even P, Bloch-Faure M, Guerre-Millo M, Moustaid-Moussa N, Ferre P, Quignard-Boulange A. Deletion of the angiotensin type 2 receptor (AT2R) reduces adipose cell size and protects from diet-induced obesity and insulin resistance. Diabetes 54 (4):991-999, 2005.
- Kim, S., Voy, B.H., Huang, T., Koontz, J.W., Quignard-Boulange, A., Hayzer, J., Harp, J.B., and Moustaid-Moussa, N. Angiotensin II uses insulin signaling pathways in 3T3-L1 adipocytes. Adipocyte 1(4): 239-248, 2005.
- Kim, S., Soltani-Bejnood, M., Massiera, F., Ailhaud, G., Teboul, M., Quignard-Boulange, A.,Moustaid-Moussa, N. and Voy, B.H. adipocyte angiotensinogen modulates insulin sensitivity and renal renin angiotensin system. J. Biomed. Biotechnol Article ID 27012, pp1-6, 2006
- Davis, J., Higginbotham, A., O'Connor, T., Moustaid-Moussa, N., Tebbe, A., Kim, Y.C., Cho, K.W., Shay, N., Adler, S., Peterson, R. and Banz, W. Soy Protein and Isoflavones Influence Adiposity and Development of Metabolic Syndrome in the Obese Male ZDF Rat. Ann Nutr Metab. 2007;51(1):42-52. Epub 2007 Mar 14.
- Dubois, M., Vacher, P., Roger, R. Huyghe, D., Vandewalle, B., Kerr-Conte, J., Pattou, F., Moustaïd-Moussa, N., and Lang, J. Glucotoxicity inhibits late steps of insulin exocytosis. Endocrinology. 2007 Apr;148(4):1605-14. Epub 2007 Jan 4.
- Yvan-Charvet, L., Massiéra, F., Lamandé, N., Ailhaud, G., Teboul, M., Moustaid-Moussa, N., Gasc, J.M. and Annie Quignard-Boulangé. Angiotensin type 2 receptor reverses obesity but not hypertension induced by overexpression of angiotensinogen in adipose tissue. Endocrinology 150: 1421–1428, 2009.
- Wortman, P, Miyazaki, Y., Kalupahana, N., Kim, S., Hansen-Petrik, M., Saxton, A., Claycombe, K., Voy, BH., Whelan J and Moustaid-Moussa, N. PUFA modulate adipocyte prostaglandin secretion and fatty acid metabolism in 3T3-L1 adipocytes. Biomed Central Nutrition & Metabolism, 6:5 doi: 10.1186/1743-7075-6-5.January 21, 2009.
- Cho, KW., Lee, OH., Banz, WJ., Moustaid-Moussa, N., Shay, N., Kim, YC. Daidzein and the daidzein metabolite, equol, enhance adipocyte differentiation and PPARg transcriptional activity.J. Nutr. Biochem. 2009