This is a NIH P30 Biomedical Research Core Center Application (RFA-OD-09-005) on Fetal Programming in the Development of Obesity-induced Cardiovascular Diseases. The request is for support of salary and start-up costs for recruit of one new investigator for appointment within the Graduate Center for Nutritional Sciences (GCNS), a multidisciplinary research and graduate program within the College of Medicine. The research area of fetal programming through dietary manipulation as a mechanism promoting obesity and cardiovascular disease in adult offspring will complement and extend an NIH funded Center of Biomedical Research Excellence (COBRE) on obesity and cardiovascular diseases. Specialized research cores, extensive University Core Facilities, and established mentoring mechanisms are in place to promote development of an independent research program towards R01 competitiveness within the research area. The new faculty recruit will be assigned dedicated research space within the highly collaborative environment of the GCNS, with availability to common use equipment and specialized cores for analytical measurements, tissue pathology, radiotelemetry measurement of blood pressure, and whole body metabolism in mice. The targeted research area complements and extends studies currently focused on identification of mechanisms linking diet-induced obesity in adults in the development of cardiovascular disease. In this sister P30 Center, new faculty recruits will examine effects of fetal programming through dietary manipulation during pregnancy on the development of obesity and cardiovascular diseases in adult offspring. Given the increasing prevalence of obesity in the US, it is important to identify the impact of maternal obesity, through consumption of a western diet, on disease development in offspring. Moreover, these sister Centers span the breadth of current research by contrasting effects of obesity during development from adult onset obesity-induced cardiovascular disease. We will use our existing strengths in mentoring and our focused research cores within the defined area of study to assure that new investigators develop independent research programs of clinical significance to the missions of NIH HLBI.

Public Health Relevance

Over 29% of child-bearing women in the US are obese. This means that the fetus is frequently exposed to dietary stimuli, including the western diet consumed by our society, during development. This proposal will hire a faculty member and provide them with the tools to establish a competitive research program in understanding the impact of dietary stimuli during pregnancy on obesity and cardiovascular diseases of adults.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Center Core Grants (P30)
Project #
1P30HL101300-01
Application #
7860955
Study Section
Special Emphasis Panel (ZHL1-CSR-E (O1))
Program Officer
Carlson, Drew E
Project Start
2009-09-30
Project End
2011-08-31
Budget Start
2009-09-30
Budget End
2010-08-31
Support Year
1
Fiscal Year
2009
Total Cost
$548,391
Indirect Cost
Name
University of Kentucky
Department
Nutrition
Type
Schools of Medicine
DUNS #
939017877
City
Lexington
State
KY
Country
United States
Zip Code
40506
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Sui, Yipeng; Park, Se-Hyung; Xu, Jinxian et al. (2014) IKK? links vascular inflammation to obesity and atherosclerosis. J Exp Med 211:869-86
Helsley, Robert N; Sui, Yipeng; Ai, Ni et al. (2013) Pregnane X receptor mediates dyslipidemia induced by the HIV protease inhibitor amprenavir in mice. Mol Pharmacol 83:1190-9
Park, Se-Hyung; Sui, Yipeng; Gizard, Florence et al. (2012) Myeloid-specific IýýB kinase ýý deficiency decreases atherosclerosis in low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol 32:2869-76
Sui, Yipeng; Ai, Ni; Park, Se-Hyung et al. (2012) Bisphenol A and its analogues activate human pregnane X receptor. Environ Health Perspect 120:399-405
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Sui, Yipeng; Xu, Jinxian; Rios-Pilier, Jennifer et al. (2011) Deficiency of PXR decreases atherosclerosis in apoE-deficient mice. J Lipid Res 52:1652-9