Department of Biological Sciences
Wehr Life Sciences, 109
1428 W. Clybourn St.
Milwaukee, WI 53233
Wehr Life Sciences, 222MilwaukeeWI53201United States of America(414) firstname.lastname@example.org
B.A. Neuroscience, 2005, University of Virginia, Charlottesville
Ph.D. Neuroscience, 2011, Northwestern University, Evanston, IL
Postdoctoral Fellow, 2011-2014, University of Cincinnati,
Postdoctoral Fellow, 2014-2016, University of Michigan, Ann ArborI
Assistant Research Scientist, Department of Surgery, University of Michigan, Ann Arbor
BIOL 3702: Experimental Physiology
The Arble laboratory uses preclinical animal models to study the neuronal links between sleep, circadian disruption, and metabolism with the long term goal of developing novel therapies for obesity, diabetes, and sleep apnea.
Circadian disruption. Humans are unique in their ability to ignore circadian signals to sleep and fast. Staying awake when your body needs to rest or eating when your body needs to fast can lead to sleep and circadian disruption. During my PhD work, I found that wild type mice fed only during the light (inactive phase) gain 2.5x more weight than those fed only during the dark (active phase). Since its publication in 2009, this manuscript has launched a new direction of circadian rhythm research which examines the links between feeding disruption and an increased risk of obesity and diabetes. Our lab examines the role of the brain in organizing circadian rhythms and how their disruption at the molecular and peripheral level can lead to impairments in metabolism, including obesity and diabetes. We are particularly interested in developing novel treatment options for night-shift workers who are at higher risk for developing cardiometabolic disease.
Sleep disruption. One of the most common forms of sleep disruption occurs in individuals with obstructive sleep apnea (OSA). During sleep, these individuals experience multiple bouts of breathing cessation per hour, resulting in brief awakenings and significant drops in blood oxygen saturation. OSA is associated with a 4-fold greater risk of mortality and affects 17% of the total population and between 40-60% of the obese population. Because of OSA’s high correlation with obesity, many have hypothesized that OSA occurs solely due to increased physical weight (e.g. fat) restricting the airway. However, our research has indicated that body weight alone does not account for sleep-disordered breathing. Instead, we find that disordered breathing is linked to impaired leptin signaling. Using preclinical mouse models and genetic approaches (e.g. DREADDs), we find that disruption of neuronal leptin signaling leads to a disordered breathing phenotype. Our laboratory receives funding from the American Heart Association to elucidate the mechanism by which neuronal leptin affects respiration and downstream cardiometabolic outcomes.
Equipment utilized by our lab: BioSpherix Oxycycler A84 with Quick and Quiet O2 Profiling: The BioSpherix OxyCycler A84 enables precise control of rapid and quiet changes of O2 levels for in vivo experiments.
2015 Sleep Research Society Early Stage Career Stage Investigator Travel and Mentorship Award
08/2017 – 07/2020
Agency: American Heart Association 17SDG33660108 (PI, Arble)
“The role of neuronal leptin in the pathogenesis, and treatment, of sleep apnea and cardiometabolic disease”
09/2012 – 09/2014
Agency: NIH/NIDDK F32 DK097867 (PI, Arble)
“Circadian disruption and bariatric surgery: impact on metabolism, clock biology”
07/2010 – 07/2011
Agency: NIH/NIA F31 AG035621 (PI, Arble)
“Aging and meal timing interact to exaggerate weight gain”
2016 Circadian disruption, sleep apnea, and metabolism: Insights from animal models. Symposium presentation, 76th Scientific Sessions of the American Diabetes Association, New Orleans, LA.
Sarah Framnes (Ph.D. student)
Dr. Arble is currently accepting new Ph.D. students into her lab