Jennifer K. Yee is a pediatric endocrinologist at Harbor-UCLA establishing her academic career studying the role of stearoyl-CoA desaturase enzyme-1 (SCD1) and fatty acid synthesis pathways in nutritional programming for obesity. As a fellow, Dr. Yee explored SCD1 inhibition using stable isotope methods under the guidance of Dr. W.N. Paul Lee. Motivated by the increasing prevalence of childhood obesity, she has directed her attention to the role of SCD1 in nutritional programming. Dr. Yee's long-term goal is to become an independent investigator and identify treatment and prevention strategies for obesity through studies on fatty acid metabolism in adipogenesis and adipocyte differentiation. Dr. Yee's immediate goal is to establish her research focus while acquiring the skills necessary for independence. Dr. Yee's proposed research activities will be supplemented by didactic education including the UCLA K30 program and the Responsible Conduct of Research course. Dr. Yee will be mentored by Dr. W.N. Paul Lee, an expert in intermediary metabolism, and Co-Sponsor Dr. Michael Ross, an expert in appetite regulation in nutritional programming. Collaborator Mina Desai will also support Dr. Yee's research training. Harbor-UCLA is an excellent academic environment for Dr. Yee, who will receive departmental and divisional support for 75% protected time, and GCRC support for her project. Clinical, laboratory, and technical environments are outstanding. The research project combines clinical and translational research studies that aim to establish the role of SCD1 in prenatal and postnatal nutritional programming. The clinical study follows newborns at risk for obesity from in utero nutritional programming over three years. Plasma fatty acid ratios representing SCD1 activity, called the desaturation indices, will be measured yearly along with body composition and biochemical markers. The parallel translational study will measure desaturation indices, and SCD1 gene and protein expression in a rat model of nutritional programming for obesity. Effects of SCD1 inhibition will be studied ex vivo in primary tissue cell culture and in vivo in the rat model. The purpose is to establish the principle that SCD1 upregulation occurs as a result of in utero programming and that inhibition of SCD1 activity can modulate development of obesity. Relevance: Too much or too little nutrition during pregnancy, called nutritional programming, can lead to offspring obesity and related problems. Changes in the fatty acid synthesis pathways from increased activity in the enzyme SCD1 have been implicated in the development of obesity, diabetes, and heart disease. The objective of this project is to establish the role of SCD1 activity in nutritional programming so that it can be studied as a target for prevention of obesity in early life.
|Yee, J K; Mao, C S; Ross, M G et al. (2014) High oleic/stearic fatty-acid desaturation index in cord plasma from infants of mothers with gestational diabetes. J Perinatol 34:357-63|
|Yee, Jennifer K; Wahjudi, Paulin N; Vega, Juan et al. (2013) Stearoyl-CoA desaturase enzyme 1 inhibition reduces glucose utilization for de novo fatty acid synthesis and cell proliferation in 3T3-L1 adipocytes. Metabolomics 9:809-816|
|Yee, Jennifer K; Phillips, Susan A; Allamehzadeh, Kambiz et al. (2012) Subcutaneous adipose tissue fatty acid desaturation in adults with and without rare adipose disorders. Lipids Health Dis 11:19|
|Wahjudi, Paulin N; K Yee, Jennifer; Martinez, Steven R et al. (2011) Turnover of nonessential fatty acids in cardiolipin from the rat heart. J Lipid Res 52:2226-33|
|Yee, Jennifer K; Lee, Wai-Nang P; Han, Guang et al. (2011) Organ-specific alterations in fatty acid de novo synthesis and desaturation in a rat model of programmed obesity. Lipids Health Dis 10:72|