The body is wired to store energy. We evolved in the cave days with little to eat – fruit maybe, an occasional successful hunt for meat or fish, so when food was available, you had better well store it because it’s infrequent. All the biochemistry of appetite and body fat metabolism and muscle tell us that this is true.
Dr. Collins's laboratory is interested in the biochemical mechanisms that regulate body weight.
Dr. Collins received her doctorate in biochemistry and drug metabolism from the Massachusetts Institute of Technology.
View All Publications
Acute stimulation of white adipocyte respiration by PKA-induced lipolysis.
Yehuda-Shnaidman E, Buehrer B, Pi J, Kumar N, Collins S
Diabetes. 2010 Oct;59(10):2474-83
Persistent oxidative stress due to absence of uncoupling protein 2 associated with impaired pancreatic beta-cell function.
Pi J, Bai Y, Daniel KW, Liu D, Lyght O, Edelstein D, Brownlee M, Corkey BE, Collins S
Endocrinology. 2009 Jul;150(7):3040-8
Reduced antioxidant capacity and diet-induced atherosclerosis in uncoupling protein-2-deficient mice.
Moukdar F, Robidoux J, Lyght O, Pi J, Daniel KW, Collins S
J Lipid Res. 2009 Jan;50(1):59-70
Orphan nuclear receptor NOR-1 enhances 3',5'-cyclic adenosine 5'-monophosphate-dependent uncoupling protein-1 gene transcription.
Kumar N, Liu D, Wang H, Robidoux J, Collins S
Mol Endocrinol. 2008 May;22(5):1057-64
Liver X receptor alpha is a transcriptional repressor of the uncoupling protein 1 gene and the brown fat phenotype.
Wang H, Zhang Y, Yehuda-Shnaidman E, Medvedev AV, Kumar N, Daniel KW, Robidoux J, Czech MP, Mangelsdorf DJ, Collins S
Mol Cell Biol. 2008 Apr;28(7):2187-200
Reactive oxygen species as a signal in glucose-stimulated insulin secretion.
Pi J, Bai Y, Zhang Q, Wong V, Floering LM, Daniel K, Reece JM, Deeney JT, Andersen ME, Corkey BE, Collins S
Diabetes. 2007 Jul;56(7):1783-91
Selective activation of mitogen-activated protein (MAP) kinase kinase 3 and p38alpha MAP kinase is essential for cyclic AMP-dependent UCP1 expression in adipocytes.
Robidoux J, Cao W, Quan H, Daniel KW, Moukdar F, Bai X, Floering LM, Collins S
Mol Cell Biol. 2005 Jul;25(13):5466-79
Persistent nuclear factor-kappa B activation in Ucp2-/- mice leads to enhanced nitric oxide and inflammatory cytokine production.
Bai Y, Onuma H, Bai X, Medvedev AV, Misukonis M, Weinberg JB, Cao W, Robidoux J, Floering LM, Daniel KW, Collins S
J Biol Chem. 2005 May 13;280(19):19062-9
p38 mitogen-activated protein kinase is the central regulator of cyclic AMP-dependent transcription of the brown fat uncoupling protein 1 gene.
Cao W, Daniel KW, Robidoux J, Puigserver P, Medvedev AV, Bai X, Floering LM, Spiegelman BM, Collins S
Mol Cell Biol. 2004 Apr;24(7):3057-67
Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation.
Cao W, Luttrell LM, Medvedev AV, Pierce KL, Daniel KW, Dixon TM, Lefkowitz RJ, Collins S
J Biol Chem. 2000 Dec 8;275(49):38131-4
Sheila Collins's Research Focus
Metabolic Diseases, Metabolic Syndrome, Obesity, Type 2 Diabetes
Watch Dr. Collins describe her research
Dr. Collins's laboratory is interested in the biochemical mechanisms that regulate body weight. Activation of the adrenaline receptors, specifically the members of the beta-adrenergic receptor (beta-AR) family, provides the major stimulus for the hydrolysis and release of stored lipids. They are also key drivers of a process called ‘nonshivering thermogenesis’ in brown fat. Brown fat cells are specialized cells rich in mitochondria and largely defined by their ability to express the mitochondrial uncoupling protein UCP1, which allows the dissipation of the proton gradient in the inner mitochondrial membrane to yield heat at the expense of ATP production.
By understanding the beta-ARs on fat cells, their signal transduction properties and how they are regulated, we hope to be able to find a way to increase energy expenditure in fat in the fight against obesity and the devastating diseases that accompany it such as diabetes, cardiovascular disease and hypertension.
About Sheila Collins
Sheila Collins, Ph.D., received her B.S. degree with honors in zoology from the University of Massachusetts at Amherst. She then joined Massachusetts General Hospital in Boston and the California Institute of Technology in Pasadena as a research technician working in developmental and molecular biology. Dr. Collins received her doctorate in biochemistry and drug metabolism from the Massachusetts Institute of Technology with Dr. Michael Marletta, and conducted postdoctoral research with Dr. Robert Lefkowitz at Duke University, both of whom are National Academy Science members. Dr. Collins continued her research career at Duke University Medical Center as a faculty member in the Department of Psychiatry and Behavioral Sciences, where she was awarded tenure. She moved to The Hamner Institutes for Health Sciences, helping to develop biomedical research, retaining her Duke faculty appointment. While there, she was named the Hamner Senior Fellow in Endocrine Biology. In 2010, Dr. Collins joined the Diabetes and Obesity Research Center at Sanford-Burnham Medical Research Institute (Orlando, FL), where she is Professor of Metabolic Disease. Dr. Collins has served on numerous review committees and advisory panels for the National Institutes of Health, the American Diabetes Association, American Heart Association and has been an organizer of many national and international scientific meetings. Dr. Collins investigates biochemical mechanisms regulating body weight. Specifically, her lab is deciphering how hormonal signals such as adrenaline and novel pathways using heart-derived hormones control fat cell metabolism, including how the genes in brown and white adipocytes are controlled to increase energy expenditure and weight loss.
Adjunct Associate Professor, Psychiatry and Behavioral Sciences, Duke University Medical Center
Adjunct Assistant Professor, Department of Medicine, Duke University Medical Center