Terry Hinds

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Associate Professor

University of Kentucky

United States

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About

Terry Hinds is an Associate Professor at the University of Kentucky. His research focuses on the intersections of liver physiology, insulin resistance, and glucocorticoid signaling, with recent studies exploring molecular pathways related to liver fibrosis and its associations with metabolic disorders. He is also investigating the role of steroid receptors in disease pathology and the impacts of novel substances on biological function. His work contributes significantly to understanding the mechanistic underpinnings of various hepatic and metabolic diseases.

Recent Grants

Grant: Close

Novel Liver Signaling Pathways Controlling Adiposity

Open Date: 2020-07-01

Close Date: 2025-06-01

Grant: Close

Antioxidant-PPARalpha interaction and hypertension

Open Date: 2014-11-15

Close Date: 2019-10-31

Grant: Close

Fatty acid Control Obesity and the Metabolic Syndrome via TPR proteins

Open Date: 2009-04-13

Close Date: 2011-04-12

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UNITED STATES

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Brett T. Spear

University of Kentucky College of Medicine

UNITED STATES

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Hunter Moseley

Professor

University of Kentucky

UNITED STATES

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Alexandre A. da Silva

University of Mississippi Medical Center

UNITED STATES

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Terry Hinds

Research Interests

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About

Recent Grants

Articles (21)

The physiology of MASLD: molecular pathways between liver and adipose tissues

Steroid receptors and coregulators: Dissemination of sex differences and emerging technologies

Insulin receptor responsiveness governs TGFβ‐induced hepatic stellate cell activation: Insulin resistance instigates liver fibrosis

Heme oxygenase, biliverdin reductase, and bilirubin pathways regulate oxidative stress and insulin resistance: a focus on diabetes and therapeutics

Urobilin Derived from Bilirubin Bioconversion Binds Albumin and May Interfere with Bilirubin Interacting with Albumin: Implications for Disease Pathology

Impacts of xylazine on fentanyl demand, body weight, and acute withdrawal in rats: A comparison to lofexidine

Human soluble prorenin receptor expressed in mouse renal collecting duct shows sex-specific effect on cardiorenal function

Glucocorticoids, their uses, sexual dimorphisms, and diseases: new concepts, mechanisms, and discoveries

FOXS1 is increased in liver fibrosis and regulates TGFβ responsiveness and proliferation pathways in human hepatic stellate cells

Glucocorticoid resistance remodels liver lipids and prompts lipogenesis, eicosanoid, and inflammatory pathways

Xylazine Suppresses Fentanyl Consumption During Self-Administration and Induces a Unique Sex-Specific Withdrawal Syndrome That Is Not Altered By Naloxone in Rats

Bilirubin Nanoparticle Treatment in Obese Mice Inhibits Hepatic Ceramide Production and Remodels Liver Fat Content

Loss of hepatic PPARα in mice causes hypertension and cardiovascular disease

The physiology of bilirubin: health and disease equilibrium.

Powering the Powerhouse: Heme Oxygenase-1 Regulates Mitochondrial Function in Non-Alcoholic Fatty Liver Disease (NAFLD).

Bilirubin Levels Are Negatively Correlated with Adiposity in Obese Men and Women, and Its Catabolized Product, Urobilin, Is Positively Associated with Insulin Resistance

Suppressing Hepatic UGT1A1 Increases Plasma Bilirubin, Lowers Plasma Urobilin, Reorganizes Kinase Signaling Pathways and Lipid Species and Improves Fatty Liver Disease

Antioxidant Therapy Significantly Attenuates Hepatotoxicity following Low Dose Exposure to Microcystin-LR in a Murine Model of Diet-Induced Non-Alcoholic Fatty Liver Disease

Editorial: Emerging talents in Frontiers in Pharmacology: Drug metabolism and transport 2022.

Zinc fingers and homeoboxes 2 is required for diethylnitrosamine‐induced liver tumor formation in C57BL/6 mice

Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways.

Collaborators (10)

Jieyun Jiang

William Stoops

Martha Peterson

Robert Helsley

Steven Haller

Analia S. Loria

Justin Fortune Creeden

Brett T. Spear

Hunter Moseley

Alexandre A. da Silva

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