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.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Center Core Grants (P30)
Project #
Application #
Study Section
Special Emphasis Panel (ZDK1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Boston Medical Center
United States
Zip Code
Tobias, D K; Zhang, C; Chavarro, J et al. (2016) Healthful dietary patterns and long-term weight change among women with a history of gestational diabetes mellitus. Int J Obes (Lond) 40:1748-1753
Huang, Ru-Yi; Huang, Chuan-Chin; Hu, Frank B et al. (2016) Vegetarian Diets and Weight Reduction: a Meta-Analysis of Randomized Controlled Trials. J Gen Intern Med 31:109-16
Zheng, Yan; Ceglarek, Uta; Huang, Tao et al. (2016) Plasma Taurine, Diabetes Genetic Predisposition, and Changes of Insulin Sensitivity in Response to Weight-Loss Diets. J Clin Endocrinol Metab 101:3820-3826
Bao, Wei; Li, Shanshan; Chavarro, Jorge E et al. (2016) Low Carbohydrate-Diet Scores and Long-term Risk of Type 2 Diabetes Among Women With a History of Gestational Diabetes Mellitus: A Prospective Cohort Study. Diabetes Care 39:43-9
Vetrivelan, Ramalingam; Kong, Dong; Ferrari, Loris L et al. (2016) Melanin-concentrating hormone neurons specifically promote rapid eye movement sleep in mice. Neuroscience 336:102-113
Shams-White, Marissa; Kelly, Michael J; Gilhooly, Cheryl et al. (2016) Food craving and obesity in survivors of pediatric ALL and lymphoma. Appetite 96:1-6
Song, Mingyang; Willett, Walter C; Hu, Frank B et al. (2016) Trajectory of body shape across the lifespan and cancer risk. Int J Cancer 138:2383-95
Chavarro, Jorge E; Mínguez-Alarcón, Lidia; Chiu, Yu-Han et al. (2016) Soy Intake Modifies the Relation Between Urinary Bisphenol A Concentrations and Pregnancy Outcomes Among Women Undergoing Assisted Reproduction. J Clin Endocrinol Metab 101:1082-90
Gaskins, Audrey J; Chiu, Yu-Han; Williams, Paige L et al. (2016) Maternal whole grain intake and outcomes of in vitro fertilization. Fertil Steril 105:1503-1510.e4
Malik, Vasanti S; Li, Yanping; Tobias, Deirdre K et al. (2016) Dietary Protein Intake and Risk of Type 2 Diabetes in US Men and Women. Am J Epidemiol 183:715-28

Showing the most recent 10 out of 762 publications