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Terry Hinds, Jr, PhD


(859) 323-3036
760 Press Avenue, Healthy Kentucky Research Building #221, Lexington, KY 40508


  • Director of the Drug & Disease Discovery D3 Research Center
  • President, Kentucky Physiological Society (KPS)
  • Associate Professor of Pharmacology and Nutritional Sciences (Tenured)
  • Director, Molecular Biological Applications in Nutrition Course
  • Graduate Faculty in Nutritional Sciences
  • Metabolism - Clinical and Experimental, Editorial board member
  • Journal of Biological Chemistry (JBC), Editorial board member
  • Acta Physiologica, Editorial board member
  • American Journal of Physiology (AJP)-Endocrinology and Metabolism, Editorial board member
  • Frontiers in Pharmacology, Editorial board member
  • Nuclear Receptor Research, Editorial board member
  • International Journal of Steroids, Editorial board member
  • Markey Cancer Center member, Molecular and Cellular Oncology (MCO) Research Program
  • Saha Cardiovascular Research Center affiliate member
  • Barnstable Brown Diabetes Center Member

College Unit(s)

Other Affiliation(s)
  • Pharmacology and Nutritional Sciences Primary Faculty
  • Nutritional Sciences Graduate Faculty
  • Markey Cancer Center - Affiliated Faculty


He, him, his

Biography and Education


Advanced Technology in the Lab

The Hinds Lab team leads cutting-edge science with the most advanced technology for studying signaling pathways: the PamGene PamStation. The Hinds Lab has specialized expertise in using this state-of-the-art instrument to measure hundreds of kinase signaling activities in a single sample, which requires much time for their lab’s extensive bioinformatic analysis. This technology is likely the future of personalized medicine, making the University of Kentucky one of the first sites globally to use this advanced instrumentation. The Hinds Lab purchased and established the equipment with startup funds and support from the Vice President of Research (VPR). UK is only the fourth site in the U.S. to have this technology. The Hinds lab is highly innovative, built for novel omic approaches using advanced technology, and welcomes collaboration.

Landmark discoveries from the lab include 1) the discovery of the murine nuclear receptor gene for glucocorticoid receptor β (GRβ) (PMID: 20660300) and the creation of all of the tools for studying this GR isoform; 2) developed the only human GRβ antagonist (Patent WO 2017155929 A1); 3) discovered that bilirubin is a hormone that activates nuclear receptors; 4) generated a bilirubin-derived molecule called Thin Molecules and patented their use for obesity and diabetes treatments (Patent Number WO 2017151469 A1); and 5) developed bilirubin nanoparticles as a therapeutic for the treatment of obesity, diabetes, and cardiovascular diseases (Patent Number WO-2020-176289 A1). Our latest work, which cannot be disclosed because of patentability, is leading-edge work where we have discovered new hormones that cause obesity-associated comorbidities.  

Hinds Lab Clinical Trial 

The Hinds Lab with Dr. Kyle Flack's lab has a Clinical Trial at the University of Kentucky where we study obese humans and whether increases in plasma bilirubin and exercise help them lose weight faster.…

Research Interests

My lab’s research is on how nutrients from the diet and hormones regulate metabolic dysfunction in obesity and diabetes. We have discovered new hormones that control the metabolic process. From these discoveries, we have generated compounds that we have patented as potential future therapeutics. Our studies open new fronts for understanding metabolic dysfunction and possible treatments.

The lab's focus is to understand the molecular mechanisms in the liver and adipose tissues that regulate fat accumulation and insulin resistance that leads to type II diabetes. We are primarily focused on nuclear receptors, heme oxygenase, and drug targeting. When a red blood cell undergoes its life span and breaks open, it releases heme that carries the oxygen. The heme oxygenase system (heme oxygenase-1, biliverdin reductase, and UGT1A1 glucuronyl enzymes) breaks the heme down to biliverdin and then bilirubin. Increasing bilirubin in the obese reduces body weight and improves insulin signaling. However, mechanisms explaining how bilirubin controls obesity and insulin resistance were unknown for nearly two decades. We discovered and established the concept that bilirubin is a metabolic hormone by binding to the nuclear receptor PPARalpha. Current investigations on how bilirubin controls metabolic dysfunction are ongoing. We have developed and patented bilirubin nanoparticles and other bilirubin-derived molecules as potential therapeutics for metabolic disease. We are working to understand the role of the proteins that regulate bilirubin's turnover, such as the enzyme that produces it, biliverdin reductase (BVR), and the glucuronyl enzyme that clears it from the body, UGT1A1. Studies have been focused on targeting these enzymes in diet-induced fatty liver disease and insulin-resistant diabetes. Together, our studies provide new avenues for drug targeting with therapeutic interventions that are translational for patient studies.

New studies are investigating an IRB-approved small clinical trial where we are using dietary supplements to increase plasma bilirubin in obese patients with and without exercise to determine if this improves weight-loss outcomes. Our studies may reveal new fronts for understanding how metabolic dysfunction and lower bilirubin affect our body's peripheral responses to fat accumulation, leading to insulin-resistant diabetes.

Areas Of Expertise

Drug design, signaling, nuclear receptors, kinases, obesity and diabetes, metabolic pathways, drug metabolism (P450 and glucuronidation enzymes), heme oxygenase and bilirubin pathway, oxidative stress, cancer-inducing pathways, and development of cancer (bladder and prostate mostly, but also others).


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.

Selected Publications

Pubmed Publications Google Scholar