Fellow Statements
Bridget Konadu
Understanding the molecular mechanisms that drive disease progression has been a central motivation throughout my scientific career. My journey began after earning my bachelor's degree, when I worked as a laboratory scientist performing diagnostic assays and interpreting patient results. Observing consistent patterns in metabolic profiles sparked my curiosity about the molecular underpinnings of metabolic disease. This curiosity led me to pursue a master's degree, which was focused on understanding the molecular mechanisms of obesity using Drosophila melanogaster as a genetic model. Through this work, we identified key GWAS candidate genes implicated in obesity pathogenesis, deepening my interest in the genetic and cellular regulation of metabolic disorders.
Building upon this foundation, my PhD focused on elucidating how fetal hyperglycemia in gestational diabetes mellitus (GDM) predisposes offspring to metabolic disease later in life. Using a zebrafish model, I identified molecular pathways linking fetal hyperglycemia to dysregulated lipid metabolism and obesity, providing new insights into how adverse perinatal exposures contribute to metabolic dysfunction in adulthood.
Currently, as a postdoctoral fellow in Dr. Joshua Speed's laboratory under the T32 training grant, I am investigating the role of endothelin-1 (ET-1) signaling in adipose tissue function and metabolic regulation. Our lab focuses on endothelial–adipocyte communication, particularly how ET-1, a potent vasoconstrictor produced by endothelial cells, contributes to adipose tissue dysfunction in obesity. My project examines how ET-1 signaling through the ETB receptor modulates adiponectin regulation and adipocyte differentiation via PPARγ-dependent pathways. Using molecular and cellular approaches, including primary adipocyte culture, pharmacological receptor inhibition, qPCR, Western blotting, immunofluorescence, and functional metabolic assays. I aim to define how ET-1/ETB signaling suppresses adipogenesis and promotes adipocyte hypertrophy.
Under the guidance of Dr. Joshua Speed, I have gained advanced technical training in primary adipocyte isolation and differentiation, gene expression analysis, fluorescence microscopy and metabolic phenotyping in mouse models of obesity. These skills have provided a strong platform for developing my independent research program.
My long-term research goal is to define how vascular-derived factors such as ET-1 regulate adipose remodeling and systemic metabolic health. Building on my current work, I plan to submit a K99/R00 Pathway to Independence Award proposal aimed at elucidating the molecular cross-talk between endothelin-1 (ET-1) signaling and estrogen receptor alpha (ERα) regulation in obesity, with a focus on determining whether these effects are mediated through the ETB receptor. This work will identify novel signaling pathways and therapeutic targets that can restore healthy adipose tissue remodeling and metabolic function.