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Dr. Collins is Professor of Cardiovascular Medicine. She received her Ph.D. degree from The Massachusetts Institute of Technology in Cambridge, MA, where she trained with Dr. Michael Marletta in biochemistry and drug metabolism. She conducted postdoctoral research at Duke University Medical Center in Durham, NC with Dr. Robert J. Lefkowitz, after which she joined the faculty of Duke University Medical Center in the Department of Psychiatry and Behavioral Science and was awarded Tenure. From 2010-2018 she was a Professor in the Diabetes, Obesity and Cardiovascular Research Center at Sanford-Burnham-Prebys Medical Institute. Dr. Collins’ research focuses on signal transduction and regulation of fat cell metabolism, including mechanisms to enhance brown fat cell energy expenditure. She has received continuous research support from the National Institutes of Health (NIH), The American Diabetes Association, American Heart Association, and pharmaceutical companies. She has organized many National and International scientific meetings in the field of obesity and metabolic disease, served as a member of grant review panels for NIH and foundations.
Brown adipose tissue (BAT) evolved as a means of generating heat from stored calories, an adaptation termed non-shivering thermogenesis (NST); it was particularly important to early humans before the advent of houses and clothing. Brown adipocytes are highly enriched in mitochondria and express uncoupling protein-1 (UCP1), a unique protein that serves to ‘uncouple’ the mitochondrial proton gradient from ATP production. These cells are avid consumers of the glucose and fatty acids to support this activity, the net result being energy expenditure. Active brown fat is now appreciated to be present in humans throughout the lifespan. Moreover, its amount, as in rodents, significantly correlates with lower body fat and greater insulin sensitivity. Therefore an increase in humans of brown fat cells and their metabolic activity could target obesity and its comorbidities. β-adrenergic receptors (βARs) and protein kinase A convey the signal from catecholamines to increase lipolysis in adipocytes and to promote the ‘browning’ of adipocytes within white fat depots. The cardiac natriuretic peptides ANP and BNP also increase lipolysis and adipose ‘browning’ through a parallel pathway via protein kinase G. An important component of adipose browning is the expansion of mitochondrial density and capacity to consume glucose and fatty acids. By understanding the components in the network of signals and their regulation we may identify new targets for clinical intervention in metabolic disease. This presentation will focus on novel mechanisms driving mitochondrial biogenesis and adipose browning and their contribution to whole body fuel homeostasis.