Mark Sleeman, PhD
Research & Publications
Biography
Extensive Research Description
Dr. Sleeman is the Head of Metabolic Research at Regeneron Pharmaceuticals in Tarrytown, New York. For the past two decades he has been interested in the interplay between insulin resistance and obesity, and more specifically the molecular mechanisms behind the regulation food intake and body weight. Recently, his research has focused on the role that gut hormones such as ghrelin and PYY play in signaling to a number of brain regions to modulate metabolic events. To that end he and his colleagues have generated a large number of genetically modified animals to study these phenotypes. Ultimately, his work may clarify the complex relationships on the role that circulating hormones play in regulation of short and long term metabolic events such as bone and mineral metabolism and food intake&body weight control.
Mark Sleeman was a recipient of a Juveniles Diabetes and Ruth Kirschstein Endocrine Fellowship at the University of Massachusetts in the laboratory of Dr Michael P. Czech where he studied mechanisms insulin-resistance/signaling. Dr Sleeman received his Ph.D. from Monash University, Australia, where he specialized in neurobiology and has published numerous papers in Type 2 Diabetes and Obesity in journals such as Nature Medicine, Nature Genetics, PNAS, Journal of Biological Chemistry and Diabetes and is a member of numerous professional societies in US.
Selected Publications
- Increased fear‐ and stress‐related anxiety‐like behavior in mice lacking tuberoinfundibular peptide of 39 residuesFegley DB, Holmes A, Riordan T, Faber CA, Weiss JR, Ma S, Batkai S, Pacher P, Dobolyi A, Murphy A, Sleeman MW, Usdin TB. Increased fear‐ and stress‐related anxiety‐like behavior in mice lacking tuberoinfundibular peptide of 39 residues. Genes Brain & Behavior 2008, 7: 933-942. PMID: 18700839, PMCID: PMC2605196, DOI: 10.1111/j.1601-183x.2008.00432.x.
- The CAMplexities of Central GhrelinSleeman MW, Latres E. The CAMplexities of Central Ghrelin. Cell Metabolism 2008, 7: 361-362. PMID: 18460326, DOI: 10.1016/j.cmet.2008.04.009.
- Hypothalamic Fatty Acid Metabolism Mediates the Orexigenic Action of GhrelinLópez M, Lage R, Saha AK, Pérez-Tilve D, Vázquez MJ, Varela L, Sangiao-Alvarellos S, Tovar S, Raghay K, Rodríguez-Cuenca S, Deoliveira RM, Castañeda T, Datta R, Dong JZ, Culler M, Sleeman MW, Álvarez C, Gallego R, Lelliott CJ, Carling D, Tschöp MH, Diéguez C, Vidal-Puig A. Hypothalamic Fatty Acid Metabolism Mediates the Orexigenic Action of Ghrelin. Cell Metabolism 2008, 7: 389-399. PMID: 18460330, DOI: 10.1016/j.cmet.2008.03.006.
- The mutation ROR2W749X, linked to human BDB, is a recessive mutation in the mouse, causing brachydactyly, mediating patterning of joints and modeling recessive Robinow syndromeRaz R, Stricker S, Gazzerro E, Clor JL, Witte F, Nistala H, Zabski S, Pereira RC, Stadmeyer L, Wang X, Gowen L, Sleeman MW, Yancopoulos GD, Canalis E, Mundlos S, Valenzuela DM, Economides AN. The mutation ROR2W749X, linked to human BDB, is a recessive mutation in the mouse, causing brachydactyly, mediating patterning of joints and modeling recessive Robinow syndrome. Development 2008, 135: 1713-1723. PMID: 18353862, DOI: 10.1242/dev.015149.
- Simultaneous deletion of ghrelin and its receptor increases motor activity and energy expenditurePfluger PT, Kirchner H, Günnel S, Schrott B, Perez-Tilve D, Fu S, Benoit SC, Horvath T, Joost HG, Wortley KE, Sleeman MW, Tschöp M. Simultaneous deletion of ghrelin and its receptor increases motor activity and energy expenditure. AJP Gastrointestinal And Liver Physiology 2007, 294: g610-g618. PMID: 18048479, DOI: 10.1152/ajpgi.00321.2007.