Current Funding Awardees

Pilot and Feasibility Awardees

Suchi Chandrasekaran, MD, MSCE
Assistant Professor
Department of Obstetrics and Gynecology

Gestational diabetes mellitus (GDM) is associated with a 6-fold increased risk for development of maternal type 2 diabetes. Identifying mechanisms that promote GDM would aid in understanding why only some women are prone to GDM. Studies in rodent models exposed to a high fat diet suggest that obesity, including increased visceral fat mass, is preceded by central nervous system inflammation and injury called gliosis in a region of the mediobasal hypothalamus (MBH) that houses neurons regulating energy and glucose homeostasis. We propose to investigate whether in humans, MBH gliosis, either directly or indirectly through increased visceral fat deposition, is a potential precursor to the development of GDM. Our data could provide the foundation for developing strategies to prevent GDM.

Dan Shao, Ph.D.
Acting Instructor
Department of Anesthesiology and Pain Medicine

Cardiovascular disease is the major cause of death in obese and diabetic patients. Structural damage and functional impairment of mitochondria contribute to obesity and diabetic heart diseases. However, very little is known about the involvement of mitochondria clearance machinery, particular mitophagy, in the pathogenesis of cardiomyopathy. We seek to understand how alterations of lipid metabolism regulate mitophagy. Our study will provide initial evidence to determine whether mitophagy can be targeted therapeutically for obesity/diabetes induced cardiomyopathy.

New Investigator Awardee

Elizabeth Rhea, Ph.D.
Research Assistant Professor
Department of Medicine

Insulin has multiple glucoregulatory roles within the central nervous system (CNS). Its transport across the blood-brain barrier (BBB) is highly regulated, yet the mechanism for transport across the brain endothelial cell and into the CNS remains unclear. We seek to determine whether internalization and binding regulation of the signaling-related insulin receptor versus the insulin transporter differ. Once we know how insulin transport and binding at the BBB is regulated, we can investigate how the process is altered under obese or diabetic conditions. Pharmacological interventions could be developed to improve the transport of insulin across the BBB in type 2 diabetes to restore insulin signaling in the CNS and improve CNS insulin resistance.

Dick and Julia McAbee Postdoctoral Fellowship Awardee

Jennifer Deem, Ph.D.
Senior Fellow
Department of Medicine

Adaptive thermoregulatory responses are centrally controlled by the hypothalamic preoptic area, including its predominant population of warm-sensitive neurons (WSN). When inhibited, these neurons allow activation of downstream sympathetic premotor neurons, increase sympathetic outflow to thermogenic tissues, and defend normal body temperature. We hypothesize that appropriate inhibition of WSN helps ensure tissue glucose needs are met in ways that preserve overall glucose homeostasis. Using two defined populations of WSN as a starting point, my work will determine their contribution to glucose homeostasis using pharmaco- and optogenetic technology in combination with state-of-the-art glucose and energy metabolic phenotyping. This work is expected to provide insights into central mechanisms that contribute to impaired glucose tolerance and its progression to type 2 diabetes.

Samuel and Althea Stroum Graduate Fellowship Awardee

Jenny Brown
Ph.D. Candidate
Department of Pathology

Our lab recently showed that a single intracerebroventricular injection of fibroblast growth factor 1 (FGF1) elicits sustained diabetes remission in rodent models of type 2 diabetes, suggesting the brain could be a key target for future diabetes drug development. Further, our data support the hypothesis that FGF1-induced diabetes remission involves activation of a FGF receptor-integrin pathway in a brain area known as the hypothalamic arcuate nucleus (ARC) and the adjacent median eminence (ME). Our proposed studies to test this hypothesis will focus on the question of whether an action in the ARC-ME is both necessary and sufficient to explain FGF1-induced diabetes remission. Our findings will identify the neurocircuitry responsible for the antidiabetic effect of FGF1, a key step in development of therapeutics.