Adipose tissue function is central to overall metabolism. In addition to its energy storage role, adipose tissue secretes bioactive factors (i.e. adipokines) that contribute to regulating food intake, energy expenditure and normal functioning of key organs such as the vasculature, muscle and liver. Excessive expansion of adipose tissue, as occurs in obesity, is associated with cardiovascular abnormalities and systemic inflammation which ultimately may promote development of cardiovascular disease, diabetes and cancer. Adipose tissue expansion involves processes that include adipocyte hypertrophy, adipogenesis (pre-adipocyte differentiation), angiogenesis (new blood vessel formation) and extracellular matrix remodeling. There is growing interest in targeting these processes as a potentially efficient way to limit adipose tissue mass and obesity. In addition, understanding the molecular mechanisms that mediate lipid storage and the nutritional effects on adipose tissue metabolism are important in the pathophysiology of obesity. The Adipocyte Biology and Molecular Nutrition (ABMN) Core was established in 2006 and has since played a central role in facilitating molecular research related to nutrition and obesity by NORC investigators. The core provides NORC researchers, especially young investigators, access to specific equipment and expertise that are difficult to assemble by individual investigators and that can present a barrier to those new to this field. The state-of-the-art research infrastructure and training available through the ABMN Core facilitate and enhance nutrition/obesity related research and maximize resource use for NORC investigators, particularly young investigators who are establishing independent research programs. The core helps clinical investigators who are interested in the mechanisms underlying the pathophysiology associated with obesity in conducting molecular studies of biopsy samples obtained from metabolically phenotyped subjects. The ABMN core also creates opportunities for interactions and collaborations that often lead to initiation of new multidiscipiinary projects and help recruit basic and clinical investigators to nutrition/obesity related research (see publication record).

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
2P30DK056341-11
Application #
8132696
Study Section
Special Emphasis Panel (ZDK1-GRB-2 (J2))
Project Start
2011-04-01
Project End
2016-03-31
Budget Start
2011-04-01
Budget End
2012-03-31
Support Year
11
Fiscal Year
2011
Total Cost
$115,134
Indirect Cost
Name
Washington University
Department
Type
DUNS #
068552207
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
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Wildburger, Norelle C; Gyngard, Frank; Guillermier, Christelle et al. (2018) Amyloid-? Plaques in Clinical Alzheimer's Disease Brain Incorporate Stable Isotope Tracer In Vivo and Exhibit Nanoscale Heterogeneity. Front Neurol 9:169
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Lutkewitte, Andrew J; Schweitzer, George G; Kennon-McGill, Stefanie et al. (2018) Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration. Food Chem Toxicol 115:273-283
Lucey, Brendan P; Hicks, Terry J; McLeland, Jennifer S et al. (2018) Effect of sleep on overnight cerebrospinal fluid amyloid ? kinetics. Ann Neurol 83:197-204
Rother, Kristina I; Sylvetsky, Allison C; Walter, Peter J et al. (2018) Pharmacokinetics of Sucralose and Acesulfame-Potassium in Breast Milk Following Ingestion of Diet Soda. J Pediatr Gastroenterol Nutr 66:466-470
Oh, Jisu; Riek, Amy E; Zhang, Rong M et al. (2018) Deletion of JNK2 prevents vitamin-D-deficiency-induced hypertension and atherosclerosis in mice. J Steroid Biochem Mol Biol 177:179-186
Riek, Amy E; Oh, Jisu; Darwech, Isra et al. (2018) Vitamin D3 supplementation decreases a unique circulating monocyte cholesterol pool in patients with type 2 diabetes. J Steroid Biochem Mol Biol 177:187-192
Bittel, Adam J; Bohnert, Kathryn L; Reeds, Dominic N et al. (2018) Reduced Muscle Strength in Barth Syndrome May Be Improved by Resistance Exercise Training: A Pilot Study. JIMD Rep :
Shepherd, Andrew J; Copits, Bryan A; Mickle, Aaron D et al. (2018) Angiotensin II Triggers Peripheral Macrophage-to-Sensory Neuron Redox Crosstalk to Elicit Pain. J Neurosci 38:7032-7057

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