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Jay D. Horton obtained his B.S. and M.D. degrees from the University of Iowa in 1984 and 1988, respectively. He completed his internal medicine residency (1988-1991) and gastroenterology fellowship (1991-1994) at UT Southwestern Medical Center. During his gastroenterology fellowship he studied metabolic regulators of bile acid and cholesterol homeostasis in animals. Following the gastroenterology fellowship, he completed a Howard Hughes post doctoral fellowship in the Department of Molecular Genetics at UT Southwestern Medical Center. The studies in this fellowship focused on the transcriptional regulation of cholesterol and fatty acid synthesis.

In clinical digestive diseases, Dr. Horton has an interest in conditions that lead to steatosis and obesity. Currently the laboratory is investigating molecular mediators of steatosis using various mouse models. Investigations from the laboratory have revealed how the primary transcriptional regulators of cholesterol metabolism (sterol regulatory element-binding proteins) are also key regulators of fatty acid synthesis in liver.

A major focus of the laboratory is to determine how these transcriptional regulators contribute to the development of steatosis in various disease processes such as diabetes, obesity, and beta-oxidation defects.

A second area of investigation centers on determining the function of PCSK9, a protein that is involved in determining plasma LDL cholesterol levels through its ability to post-transcriptionally regulate the expression of the LDL receptor in liver.


Medical School
University of Iowa Hospitals and Clinics (1988)
Parkland Health & Hospital System (1991), Internal Medicine
UT Southwestern Medical Center (1994), Gastroenterology
UT Southwestern Medical Center (1997), Molecular Genetics

Research Interest

  • Hepatic steatosis
  • Lipid metabolism


Featured Publications LegendFeatured Publications

Acetyl CoA Carboxylase Inhibition Reduces Hepatic Steatosis but Elevates Plasma Triglycerides in Mice and Humans: A Bedside to Bench Investigation.
Kim CW, Addy C, Kusunoki J, Anderson NN, Deja S, Fu X, Burgess SC, Li C, Ruddy M, Chakravarthy M, Previs S, Milstein S, Fitzgerald K, Kelley DE, Horton JD Cell Metab. 2017 Aug 26 2 394-406.e6
Inhibition of PCSK9 does not improve lipopolysaccharide-induced mortality in mice.
Berger JM, Loza Valdes A, Gromada J, Anderson N, Horton JD J. Lipid Res. 2017 Jun
Expression of SREBP-1c requires SREBP-2-mediated generation of a sterol ligand for LXR in livers of mice.
Rong S, Cortés VA, Rashid S, Anderson NN, McDonald JG, Liang G, Moon YA, Hammer RE, Horton JD Elife 2017 Feb 6
A Highly Durable RNAi Therapeutic Inhibitor of PCSK9.
Fitzgerald K, White S, Borodovsky A, Bettencourt BR, Strahs A, Clausen V, Wijngaard P, Horton JD, Taubel J, Brooks A, Fernando C, Kauffman RS, Kallend D, Vaishnaw A, Simon A N. Engl. J. Med. 2016 Nov
AGPAT2 is essential for postnatal development and maintenance of white and brown adipose tissue.
Cautivo KM, Lizama CO, Tapia PJ, Agarwal AK, Garg A, Horton JD, Cortés VA Mol Metab 2016 Jul 5 7 491-505

Honors & Awards

  • NIH INMP Study Section Ad Hoc
  • American Association of Clinical Endocrinologists Frontiers in Science Award
  • American Society for Clinical Investigation
    Council Member (2015-2018)
  • Association of American Physicians
  • American Society for Clinical Investigation
  • Established Investigator
    American Heart Foundation (2000)
  • PEW Scholar
    PEW Foundation (2000)
  • Research Scholar Award
    American Digestive Health Foundation (1999)