Katherine Motyl, PhD

Faculty Scientist II


BA: Chemistry & Biology, Kalamzoo College
PhD: Physiology, Michigan State University

Motyl Lab 

Furthering our understanding of the brain-bone-metabolism connection.

The Motyl laboratory is broadly interested in how the nervous system regulates bone turnover. Bone is a dynamic tissue, which is constantly being broken down (bone resorption) and rebuilt (bone formation). Many local and systemic factors regulate bone turnover, including signals from the nervous system. We have specific interests in understanding the role of bone-resorbing osteoclasts in neural-mediated bone changes, and identifying feedback loops regulating neural output to bone. Our work has implications for the natural aging process, as well as for people taking medications that influence the central nervous system, like β-blockers and opioids.

Motyl Lab Osteoclast

Confocal image of an osteoclast expressing β-adrenergic receptor. Cells were isolated from the bone marrow of 6-week old mice and cultured for five days in osteoclast-differentiation media. Images were acquired at 63x magnification and staining was performed for the following: DAPI (nucleus; blue), Phalloidin (F-actin; green), and β-adrenergic receptor (anti-β-adrenergic receptor antibody; red). Pictured are three individual fluorescence channels and a composite overlay of all channels (bottom right corner). Osteoclasts form when precursor cells fuse together, resulting in large multinucleated cells that form a “sealing zone” and release several factors that break down the bone matrix.

To learn more about these and other projects in the Motyl lab, please see our publications or contact Dr. Motyl directly at motylk@mainehealth.org. You can also follow the lab on Twitter at @MotylLab.

Motyl Lab Members



Kevin Huang

Student II

Kevin Huang, BS, MPH, OMS-II, is a second-year medical student in the Motyl lab. He obtained his BS in Biology and his MPH at the University of Massachusetts in Lowell in 2018, and is currently studying osteopathic medicine at the University Of New England College Of Osteopathic Medicine. Kevin’s research focuses on opioid use in conjunction with other fracture-associated drugs. Kevin is studying how selective serotonin reuptake inhibitors (SSRIs) further increase opioid-induced fracture-risk. Kevin’s modeling of pharmaceutical-induced changes in bone metabolism will lead to clinical mitigation strategies for bone loss and fracture prevention.

Audrie Langlais

Graduate Student


Audrie Langlais, BS, is a second-year graduate student in the Motyl Lab, receiving training for a PhD in Biomedical Science from The University of Maine. She received her BS in Biochemistry from the University of New England and joined the lab in 2018 as a Research Assistant. Audrie’s research focuses on a population of cold-detecting sensory neurons that express Trpm8 (transient potential cation channel subfamily M member 8) which the lab has found are important for skeletal homeostasis. Sensory neurons receive and relay signals from peripheral environment to the central nervous system to initiate adaptive responses. Audrie will use genetically engineered mouse models to determine mechanisms of TRPM8 signaling in bone.

Bilan Mohamed


Bilan Mohamed is an intern in the Motyl Lab. Bilan is an undergraduate student at the University of Southern Maine, where she is pursuing a B.S in Biology with a concentration in Human Studies as well as a double minor in Biochemistry and Psychology. She is investigating changes in bone resorption and formation using techniques to quantify changes in gene expression in the tibia, cortical bone, and bone marrow of β1AR conditional knockout models.

Becky Mountain

Postdoctoral Research Fellow

Becky Mountain, PhD, is a postdoctoral research fellow in the Motyl Lab. She completed her PhD in Anthropology at the University of Arizona in 2019. Her research interests focus on the mechanisms of how the sympathetic nervous system, and how psychosocial stress specifically, impact skeletal metabolism and bone loss on both individual and evolutionary scales. In the Motyl Lab, Becky will be working on a project exploring how osteoclasts may provide feedback to the sensory nerves via calcium signaling to regulate bone metabolism.

Ryan Neilson

Research Assistant III

Ryan Neilson, BS, is a research assistant in the Motyl Lab. He completed his BS in Biology at the University of Southern Maine. He is interested in the mechanisms involved in beta-adrenergic signaling via sympathetic nervous system activation and the receptors that influence bone resorption. His research focuses on investigating the role of the β1AR, and how it may directly promote osteoclast differentiation.

Becca Peters

Graduate Student

Becca Peters, BS, is a University of Maine Biomedical Science PhD student in the Motyl Lab. She completed her BS at the University of New Haven, double majoring in Forensic Science and Biology in 2019. Her research will focus on the role of βAR signaling in osteoclasts. She will test the contribution of osteoclast βARs to sympathetic nervous system and age-related mediated bone loss in vivo. She will also study how clinically prescribed β-blockers influence osteoclast function.



A complete list of publications can be found on My NCBI

Original Manuscripts:

Motyl KJ, Beauchemin M, Barlow D, Le PT, Nagano K, Treyball A, Contractor A, Baron R, Rosen CJ, Houseknecht KL. A novel role for dopamine signaling in the pathogenesis of bone loss from the atypical antipsychotic drug risperidone in female mice. Bone. 2017; 103:168-176. PMID: 28689816

Carvalho AL, DeMambro VE, Guntur AR, Le P, Nagano K, Baron R, de Paula FJA, Motyl KJ. High fat diet attenuates hyperglycemia, body composition changes, and bone loss in male streptozotocin-induced type 1 diabetic mice. Journal of Cellular Physiology. 2017; PMID: 28631813

Irwin R, Lin HV, Motyl KJ, McCabe LR. Normal bone density obtained in the absence of insulin receptor expression in bone. Endocrinology. 147(12):5760-5767, 2006. Highlighted in Endocrine News

Motyl KJ and LR McCabe. Leptin treatment prevents type I diabetic marrow adiposity but not bone loss in mice. J Cell Physiol. 218(2): 376-384, 2009. Highlighted in Science Now http://news.sciencemag.org/sciencenow/2010/03/appetite-suppressor-could-be-an-.html

Motyl KJ*, S Botolin*, R Irwin*, T Kadakia, A Amalfitano, RC Schwartz, and LR McCabe. Bone inflammation and altered gene expression with type I diabetes early onset. J Cell Physiol. 218(3):575-583. *authors contributed equally

Motyl KJ, and LR McCabe. Streptozotocin, type I diabetes severity and bone. Biological Procedures Online. Published online: 06 March 2009.

Motyl KJ, Raetz M, Tekalur SA, Schwartz RC, McCabe LR. CCAAT/enhancer binding protein beta-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption. Am J Physiol Regul Integr Comp Physiol. 2011;300(5):R1250-60.

Motyl KJ, McCauley LK, McCabe LR. Amelioration of Type I Diabetes-induced Osteoporosis by Parathyroid Hormone is Associated with Improved Osteoblast Survival. J Cell Physiol. 2012 Apr;227(4):1326-34.

Motyl KJ*, Dick-de-Paula I*, Maloney AE, Lotinun S, Bornstein S, de Paula FJ, Baron R, Houseknecht KL, Rosen CJ. Trabecular bone loss after administration of the second-generation antipsychotic risperidone is independent of weight gain. Bone. 2012;Feb;50(2):490-8. *authors contributed equally

Motyl KJ, Bishop KA, Demambro VE, Bornstein SA, Le P, Kawai M, Lotinun S, Horowitz MC, Baron R, Bouxsein ML, Rosen CJ. Altered thermogenesis and impaired bone remodeling in Misty mice. J Bone Miner Res. 2013. 28(9):1885-97. PMCID: PMC3743939.

Devlin MJ, Van Vliet M, Motyl K, Karim L, Brooks DJ, Louis L, Conlon C, Rosen CJ, Bouxsein ML. Early-onset type 2 diabetes impairs skeletal acquisition in the male TALLYHO/JngJ mouse. Endocrinology. 2014. Oct;155(10):3806-16. PMCID: PMC4164927.

Motyl KJ, DeMambro VE, Barlow D, Olshan D, Nagano K, Baron R, Rosen CJ, Houseknecht, CJ. Propranolol attenuates trabecular bone loss in female mice from the atypical antipsychotic, risperidone. Endocrinology. 2015; 156(7):2374-83. PMID: 25853667. **highlighted in Endocrine News.

Zhang J, Motyl KJ, Irwin R, MacDougald OA, Britton RA and McCabe LR. Loss of bone and Wnt10b expression with type 1 diabetes is blocked by the probiotic L. reuteri. Endocrinology. 2015; 156(9):3169-82.

Review Publications

Rosen CJ, Motyl KJ. No bones about it: insulin modulates skeletal remodeling. Cell. 2010;142(2):198-200.

Motyl KJ, McCabe LR, Schwartz AV. Bone and glucose metabolism: A two-way street. Arch Biochem Biophys. 2010 Nov 1;503(1):2-10.

Motyl KJ, Rosen CJ. Temperatures rising: Brown fat and bone. Discov Med. 2011 Mar;11(58):179-85.

Motyl KJ, Rosen CJ. Understanding leptin-dependent regulation of skeletal homeostasis. Biochimie. 2012 Oct;94(10):2089-96.

Motyl KJ, Rosen CJ. The skeleton and the sympathetic nervous system: it’s about time! J Clin Endocrinol Metab. 2012 Nov;97(11):3908-11.

Calarge CA, Ivins SD, Motyl KJ, Shibli-Rahhal AA, Bliziotes MM, and Schlechte JA. Possible mechanisms for the skeletal effects of antipsychotics in children and adolescents. Therapeutic Advances in Psychopharmacology. 3(5): 278-93. 2013. PMCID: PMC3805387.

Academic Appointments

  • Faculty Scientist I, MaineHealth Institute for Research, Scarborough, ME
  • Graduate Faculty, Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME
  • Assistant Professor, Department of Medicine, Tufts University School of Medicine, Boston, MA.

Professional Activities

  • Member, Editorial Board, Endocrinology
  • Member, American Association for the Advancement of Science
  • Member, American Society for Bone and Mineral Research
  • Member, The Endocrine Society
  • Member, Society for Neuroscience

The Motyl Lab Science Sketch video below demonstrates how the metabolic consequences of antipsychotic drugs relate to changes in bone remodeling.