Vanderbilt University School of Medicine

Ellacott, Kate L.J. , PhD

Lab Url:

Phone Number: 936-8143


Ellacott, Kate's picture

Office Address   Mailing Address

Office: 8425D MRB IV Lab: 8415 MRB IV

702 Light Hall 37232

Research Keywords

Research Specialty
The effect of obesity on central nervous system function.

Research Description
Our goal is to understand how obesity affects the central nervous system (CNS). In the periphery, obesity is associated with chronic low-grade inflammation which in turn is linked to a significant increase in the incidence of diabetes, cardiovascular disease, and a variety of cancers. Mounting evidence from clinical studies suggests that obesity is associated with increased vulnerability of the CNS to damage from acute and chronic insults such as stroke and dementia. Currently, little is known about the mechanisms underlying this phenomenon but we hypothesize that obesity related changes in the neuroimmune milieu may be a contributing factor. The energy homeostasis field has largely focused on the role of neurons in both the pathogenesis and pathophysiology of obesity and the specific contribution of other CNS cell types has remained largely unexamined. Our laboratory is interested in how obesity affects non-neuronal cell types in the CNS such as glia and cerebral endothelial cells. We employ a variety of techniques including neuroanatomy, in vivo physiology, cell culture and molecular biology.

Buckman, LB, Hasty, AH, Flaherty, DK, Buckman, CT, Thompson, MM, Matlock, BK, Weller, K, Ellacott, KL. Obesity induced by a high-fat diet is associated with increased immune cell entry into the central nervous system. Brain Behav Immun, , , 2013.

Buckman, LB, Thompson, MM, Moreno, HN, Ellacott, KL. Regional astrogliosis in the mouse hypothalamus in response to obesity. J Comp Neurol, 521(6), 1322-33, 2013.

Pendergast, JS, Branecky, KL, Yang, W, Ellacott, KL, Niswender, KD, Yamazaki, S. High-fat diet acutely affects circadian organisation and eating behavior. Eur J Neurosci, 37(8), 1350-6, 2013.

Hatoum, IJ, Stylopoulos, N, Vanhoose, AM, Boyd, KL, Yin, DP, Ellacott, KL, Ma, LL, Blaszczyk, K, Keogh, JM, Cone, RD, Farooqi, IS, Kaplan, LM. Melanocortin-4 receptor signaling is required for weight loss after gastric bypass surgery. J Clin Endocrinol Metab, 97(6), E1023-31, 2012.

Orr, JS, Puglisi, MJ, Ellacott, KL, Lumeng, CN, Wasserman, DH, Hasty, AH. Toll-like receptor 4 deficiency promotes the alternative activation of adipose tissue macrophages. Diabetes, 61(11), 2718-27, 2012.

Renquist, BJ, Murphy, JG, Larson, EA, Olsen, D, Klein, RF, Ellacott, KL, Cone, RD. Melanocortin-3 receptor regulates the normal fasting response. Proc Natl Acad Sci U S A, 109(23), E1489-98, 2012.

Renquist, BJ, Lippert, RN, Sebag, JA, Ellacott, KL, Cone, RD. Physiological roles of the melanocortin MC(3) receptor. Eur J Pharmacol, 660(1), 13-20, 2011.

Srisai, D, Gillum, MP, Panaro, BL, Zhang, XM, Kotchabhakdi, N, Shulman, GI, Ellacott, KL, Cone, RD. Characterization of the Hyperphagic Response to Dietary Fat in the MC4R Knockout Mouse. Endocrinology, 152(3), 890-902, 2011.

Ellacott, KL, Morton, GJ, Woods, SC, Tso, P, Schwartz, MW. Assessment of feeding behavior in laboratory mice. Cell Metab, 12(1), 10-7, 2010.

Kennedy, AJ, Ellacott, KL, King, VL, Hasty, AH. Mouse models of the metabolic syndrome. Dis Model Mech, 3(3-4), 156-66, 2010.

Ellacott, KL, Murphy, JG, Marks, DL, Cone, RD. Obesity-induced inflammation in white adipose tissue is attenuated by loss of melanocortin-3 receptor signaling. Endocrinology, 148(12), 6186-94, 2007.

Voss-Andreae, A, Murphy, JG, Ellacott, KL, Stuart, RC, Nillni, EA, Cone, RD, Fan, W. Role of the central melanocortin circuitry in adaptive thermogenesis of brown adipose tissue. Endocrinology, 148(4), 1550-60, 2007.

Ellacott, KL, Cone, RD. The role of the central melanocortin system in the regulation of food intake and energy homeostasis: lessons from mouse models. Philos Trans R Soc Lond B Biol Sci, 361(1471), 1265-74, 2006. PMCID:1642695

Ellacott, KL, Halatchev, IG, Cone, RD. Characterization of leptin-responsive neurons in the caudal brainstem. Endocrinology, 147(7), 3190-5, 2006.

Ellacott, KL, Halatchev, IG, Cone, RD. Interactions between gut peptides and the central melanocortin system in the regulation of energy homeostasis. Peptides, 27(2), 340-9, 2006.

Ellacott, KL, Donald, EL, Clarkson, P, Morten, J, Masters, D, Brennand, J, Luckman, SM. Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor. Peptides, 26(4), 675-81, 2005.

Ellacott, KL, Cone, RD. The central melanocortin system and the integration of short- and long-term regulators of energy homeostasis. Recent Prog Horm Res, 59, 395-408, 2004.

Fan, W, Ellacott, KL, Halatchev, IG, Takahashi, K, Yu, P, Cone, RD. Cholecystokinin-mediated suppression of feeding involves the brainstem melanocortin system. Nat Neurosci, 7(4), 335-6, 2004.

Halatchev, IG, Ellacott, KL, Fan, W, Cone, RD. Peptide YY3-36 inhibits food intake in mice through a melanocortin-4 receptor-independent mechanism. Endocrinology, 145(6), 2585-90, 2004.

Ellacott, KL, Lawrence, CB, Pritchard, LE, Luckman, SM. Repeated administration of the anorectic factor prolactin-releasing peptide leads to tolerance to its effects on energy homeostasis. Am J Physiol Regul Integr Comp Physiol, 285(5), R1005-10, 2003.

Ellacott, KL, Lawrence, CB, Rothwell, NJ, Luckman, SM. PRL-releasing peptide interacts with leptin to reduce food intake and body weight. Endocrinology, 143(2), 368-74, 2002.

Lawrence, CB, Ellacott, KL, Luckman, SM. PRL-releasing peptide reduces food intake and may mediate satiety signaling. Endocrinology, 143(2), 360-7, 2002.

Postdoctoral Position Available

Postdoctoral Position Details

Updated Date

Vanderbilt University is committed to principles of equal opportunity and affirmative action.
Copyright 2008 Vanderbilt University School of Medicine
The office of Biomedical Research Education & Training All rights reserved.
For questions or problems concerning this page, please submit a help ticket.