Terry D. Hinds, Jr, PhD

  • Director of the Drug & Disease Discovery D3 Research Center

  • President, Kentucky Physiological Society (KPS)

  • Professor of Pharmacology and Nutritional Sciences (Tenured)

  • Editorial board member, Metabolism Clinical & Experimental

  • Editorial board member, Journal of Biological Chemistry (JBC)

  • Editorial board member, Clinical Science

  • Editorial board member, Acta Physiologica

  • Editorial board member, Gastroenterology Report

  • Editorial board member, Frontiers in Pharmacology

  • Director, Molecular Biological Applications in Nutrition Course

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Contact

(859) 323-3036
tdhi230@uky.edu
760 Press Avenue, Healthy Kentucky Research Building #221, Lexington, KY 40508

About Terry D. Hinds, Jr, PhD

Advanced Discovery Technologies and Precision Medicine

The Hinds Laboratory serves as the scientific engine of the Drug & Disease Discovery (D3) Research Center at the University of Kentucky, a translational research enterprise dedicated to redefining how diseases are understood, diagnosed, and treated. Our mission is to uncover previously unrecognized biological pathways that drive human disease and translate these discoveries into precision therapeutics, personalized medicine strategies, and next-generation technologies. By integrating molecular biology, systems physiology, artificial intelligence, bioinformatics, and drug discovery, we pursue transformative science that can change clinical practice and establish entirely new areas of investigation. 

The laboratory is internationally recognized for pioneering advanced signaling and nuclear receptor technologies. As one of only a handful of centers in the United States using the PamGene PamStation platform, the Hinds Lab specializes in high-dimensional kinome profiling that measures hundreds of kinase activities simultaneously from a single biological specimen. These technologies allow direct measurement of pathway activity rather than prediction from gene expression alone, creating a functional map of disease mechanisms and therapeutic responses. Through computational pipelines and systems-level bioinformatic analysis, our team transforms complex signaling data into actionable biological insight. 

Most notably, the Hinds Lab developed the foundational methodologies that enabled the use of PamGene's Nuclear Hormone Receptor (NHR) PamChip technology in biological tissues and disease models. Through this work, the laboratory became the exclusive academic collaborator for the NHR PamChip platform, a unique technology that quantifies interactions between nuclear receptors and 155 coregulator motifs in real time. This capability provides an unprecedented functional view of hormone action, drug response, and transcriptional regulation. Today, the Hinds Laboratory is recognized as a world leader in nuclear receptor coregulator biology and functional kinome signaling network analysis. 

Our vision extends beyond pathway discovery. We are pioneering a new precision medicine framework that integrates kinome profiling, artificial intelligence, and predictive computational modeling. This work led to the development of the patented "Clinical Trial on a PamChip" platform, a technology designed to predict therapeutic responsiveness by measuring pathway activity directly from patient-derived biological samples. 

Landmark Scientific Discoveries

The Hinds Laboratory is distinguished by a history of discoveries that have challenged prevailing scientific dogma and created new fields of investigation.

Among the most transformative was the discovery that bilirubin is not merely a waste product of heme metabolism, but functions as a metabolic hormone and endogenous nuclear receptor ligand. This work fundamentally altered understanding of hepatobiliary physiology and established a new paradigm linking bilirubin signaling to obesity, diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD), cardiovascular disease, kidney disease, and cardiovascular-kidney-metabolic (CKM) syndrome. These discoveries launched a rapidly expanding international research field, generated multiple patents, and established new therapeutic opportunities for metabolic disease. 

Other landmark achievements include:

  • Discovery of the murine glucocorticoid receptor beta (GRβ) gene and development of the first experimental platform for studying its biological function. 
  • Development of the world's only reported GRβ-specific antagonist, resulting in international patent protection and novel therapeutic applications. 
  • Discovery that bilirubin directly activates nuclear receptor signaling pathways regulating energy metabolism and mitochondrial function. 
  • Creation of bilirubin-derived therapeutic compounds and nanotechnologies for obesity, diabetes, fatty liver disease, and cardiovascular disorders. 
  • Development of AI-guided signaling and kinome platforms designed to advance precision medicine and therapeutic development. 

*Several additional discoveries with substantial translational and commercial potential remain under active intellectual property protection. 

Research Vision

Our research seeks to answer a provocative question: What if the molecules traditionally dismissed as metabolic byproducts are actually master regulators of human physiology?

This question led to the discovery that bilirubin functions as a metabolic hormone and continues to drive our investigations into nutrient sensing, hormone signaling, metabolism, and disease pathogenesis. We focus on identifying previously unrecognized signaling networks governing obesity, insulin resistance, MASLD, cardiovascular disease, kidney disease, addiction biology, and aging. By combining advanced omics, kinomics, nuclear receptor biology, artificial intelligence, and translational physiology, we aim to uncover new biological principles and transform them into therapies that improve human health. 

Areas of Expertise

  • Metabolism, obesity, diabetes, and CKM syndrome
  • Hepatobiliary biology and MASLD/MASH
  • Nuclear receptors and transcriptional regulation
  • Kinome profiling and systems signaling biology
  • Precision medicine and AI-enabled drug discovery
  • Drug metabolism and xenobiotic responses
  • Bilirubin and heme oxygenase biology
  • Cardiovascular and renal disease mechanisms
  • Cancer signaling and therapeutic targeting
  • Translational therapeutics and biotechnology innovation
  • Multi-omics integration and bioinformatics
  • Biomarker discovery and personalized medicine

Research

The Hinds lab investigates nuclear receptors, which are ligand-activated transcription factors that serve as a large family of drug targets. We have been studying how nutrients from the diet and stress hormones (glucocorticoids, e.g., cortisol) regulate metabolic dysfunction in obesity and insulin-resistant diabetes. Recently, we found that bilirubin, a metabolite of the heme oxygenase pathway, is a ligand for the nutrient receptor PPAR alpha, which is a nuclear receptor transcription factor that drives gene expression. This was a surprising find that changed the paradigm of the biology of bilirubin and gave a new look to a well-studied molecule - that it has a hormonal function. We have designed drugs based on this premise and have been working to further understand the hormonal function of bilirubin and how it protects from obesity, insulin-resistant diabetes, and fatty liver disease. We have generated novel drugs from bilirubin and patented these technologies, such as ‘bilirubin nanoparticles’ (International patent number: WO2020/176289A1) and ‘Thin Molecules’ (International patent number: WO2017151469 A1). Projects in the lab are currently testing these unique molecules and their uses in pre-clinical models of fatty liver disease, obesity, insulin-resistant diabetes, and cardiovascular disease. There are exciting things to come.

Other work in the Hinds lab has also looked at why there are metabolic and stress hormone imbalances in the liver and brain in the obese and addicts. We discovered the glucocorticoid receptor beta (GRbeta) isoform in mice in prior work in the lab. GRbeta does not bind to glucocorticoids (cortisol and others), and high expression of GRbeta inhibits the glucocorticoid-binding isoform, GRalpha, causing glucocorticoid resistance. We have developed novel technologies for studying this isoform. Our studies on the human GRbeta isoform lead to the first and only anti-GRbeta compound that can reverse the glucocorticoid-resistance, and we patented this technology (International Patent Number: WO 2017155929 A1). In recent studies, we have shown a differential expression of GRbeta and GRalpha in brain regions of alcohol-preferring rats. Others have demonstrated that drug-targeting of PPAR nuclear receptor pathways are beneficial in insulin-resistant diabetes and addiction. The later was an unexpected find that has open new avenues of possible therapeutics. We are interested in how the GR and PPAR isoforms regulate obesity and drug dependence.