The adipocyte is now recognized as central player in the hormonal and metabolic regulation of systemic metabolism and energy balance. The size and hence the capacity of the adipose organ for energy storage is regulated by its ability to expand via increases in the size and number of adipocytes. Remodeling of adipose tissue in which older, dysfunctional adipocytes are replaced by new, smaller and insulin sensitive adipocytes, appears to be required to maintain the 'health' and 'optimal function' of the tissue. The mechanisms that regulate the recruitment of adipose progenitors and their differentiation into adipocytes are rapidly being unraveled. BNORC investigators, through efforts that have been fostered and facilitated by the Adipocyte Core outlined herein, have made substantial contributions to our understanding of adipogenesis and the role of the adipocyte and adipose tissue in nutrient metabolism. Metabolically important tissues possess highly sensitive biochemical systems for sensing the availability of specific nutrients and changes in the hormonal environment (e.g. insulin, catecholamines) via specific signaling receptors and transcriptional regulators. Furthermore, via hormone production (e.g. leptin and adiponectin), the adipocyte sends signals to the brain about the status of energy stores, and to the brown adipose tissue, liver, muscle and bone to coordinate systemic nutrient homeostasis, regulating body composition and immune function. Additional signals originate in muscle (e.g. irisin), liver and immune cells add to the complexity of metabolic regulation that influences white adipose tissue function. Dysfunction of these metabolic and endocrine loops plays a direct role in the pathogenesis of many chronic diseases, including obesity, type 2 diabetes, atherosclerosis and osteoporosis. Clearly, deeper understanding of the basic biology of adipocyte nutrient metabolism and hormone production, and how alterations in diet quantity and quality affect these organ networks is essential to the prevention and treatment of obesity and related diseases. The research needs of BNORC investigators have progressively expanded beyond the adipocyte per se, where the Adipocyte Core has historically focused most of its efforts. Thus, we have renamed our 'Adipocyte Core' o include a basic characterization of whole body glucose metabolism and immunometabolism. The purpose of the Adipose Tissue Biology and Nutrient Metabolism Core is to: 1. Facilitate and foster research on mechanisms regulating white, brite (cells in white adipose tissue with metabolic characteristics of brown) and brown adipose tissue mass, distribution, nutrient signaling and depot-specific metabolic and endocrine functions in health and disease. 2. Provide easy and cost-effective accesse to carefully quality controlled rodent and human preadipocytes and adipocytes, and banked cell and tissues and their products (e.g. RNA, cDNA, tissue or cell lysates, conditioned media). 3. Develop and standardize methods in adipocyte biology as needed by our research base in this rapidly evolving field. 4. Provide consultative advice, support and training for new investigators and established investigators from the nutrition and obesity fields, as well as other fields who wish to understand the role of adipose tissues and adipocytes in their clinical/translational studies or model systems. 5. Facilitate and foster the translation of basic research findings from cell and animal models into clinical/translational studies. 6. Organize the Adipose and Metabolic Tissue Seminar Series, which serves as an incubator for new collaborations, and as a training ground for pre-doctoral students and post-doctoral fellows. 7. Organize workshops on controversial topics and the application of new technologies to our field.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
4P30DK046200-24
Application #
9044761
Study Section
Special Emphasis Panel (ZDK1)
Project Start
Project End
Budget Start
2016-04-01
Budget End
2017-03-31
Support Year
24
Fiscal Year
2016
Total Cost
Indirect Cost
Name
Boston Medical Center
Department
Type
DUNS #
005492160
City
Boston
State
MA
Country
United States
Zip Code
Dong, Kimberly R; Tang, Alice M; Stopka, Thomas J et al. (2018) Food acquisition methods and correlates of food insecurity in adults on probation in Rhode Island. PLoS One 13:e0198598
Keum, NaNa; Ha, Kyoung Hwa; Bao, Ying et al. (2018) Long-term patterns of fasting blood glucose levels and pancreatic cancer incidence. Cancer Causes Control 29:135-142
Heianza, Yoriko; Sun, Dianjianyi; Ma, Wenjie et al. (2018) Gut-microbiome-related LCT genotype and 2-year changes in body composition and fat distribution: the POUNDS Lost Trial. Int J Obes (Lond) 42:1565-1573
Sun, D; Wang, T; Heianza, Y et al. (2018) Birthweight and cardiometabolic risk patterns in multiracial children. Int J Obes (Lond) 42:20-27
Killion, Elizabeth A; Reeves, Andrew R; El Azzouny, Mahmoud A et al. (2018) A role for long-chain acyl-CoA synthetase-4 (ACSL4) in diet-induced phospholipid remodeling and obesity-associated adipocyte dysfunction. Mol Metab 9:43-56
Leitner, Brooks P; Weiner, Lauren S; Desir, Matthew et al. (2018) Kinetics of human brown adipose tissue activation and deactivation. Int J Obes (Lond) :
Gaskins, Audrey J; Rich-Edwards, Janet W; Williams, Paige L et al. (2018) Pre-pregnancy caffeine and caffeinated beverage intake and risk of spontaneous abortion. Eur J Nutr 57:107-117
Hansen, S; Halldorsson, T I; Olsen, S F et al. (2018) Birth by cesarean section in relation to adult offspring overweight and biomarkers of cardiometabolic risk. Int J Obes (Lond) 42:15-19
Maldonado-Cárceles, Ana B; Mínguez-Alarcón, Lidia; Mendiola, Jaime et al. (2018) Meat intake in relation to semen quality and reproductive hormone levels among young men in Spain. Br J Nutr :1-10
Han, Liyuan; Duan, Donghui; Zhang, Shuang et al. (2018) Effects of the interaction between glycated haemoglobin genetic risk score and postpartum weight reduction on glycaemic changes: A gene-weight interaction analysis. Diabetes Obes Metab 20:2733-2739

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