My research over the past decade has focused on the pathogenesis of the metabolic syndrome, type 1 diabetes, and type 2 diabetes mellitus.

My work has established that the abnormalities of heat shock proteins (HSPs) in these diseases is paramount to understanding their pathogenesis. In insulin resistant states and diabetes, heat shock factor 1 (HSF-1) is low in insulin sensitive tissues, resulting in low HSP levels. Low HSPs make organs vulnerable to injury, impair the stress response, accelerate systemic inflammation, raise islet amyloid polypeptide, and increase insulin resistance. Feeding this cycle are excess saturated fat and calorie consumption, hypertension, inactivity, aging, and genetic predisposition - all of which are associated with high GSK-3 activity and low HSPs. Recognizing GSK-3 and HSPs in the pathogenesis of insulin resistance, the central common feature of the metabolic syndrome, and type 2 diabetes will expand our understanding of the disease, offering new therapeutic options.

Recent publications

P.L. Hooper, L.E. Hightower, P.L. Hooper (2012) Loss of stress response as a consequence of viral infection: Implications for disease and therapy, Cell Stress and Chaperones, published online 14 July, 2012.

Z. Literati-Nagy, K. Tory, B. Literati-Nagy, A. Kolonics, Z. Torok, I. Gombos, G. Balogh, L. Vígh Jr., I. Horvath, J. Mandl, B. Sumegi, P.L. Hooper, L. Vígh (2012) The HSP co-inducer BGP-15 can prevent the metabolic side effects of the atypical antipsychotics, Cell Stress and Chaperones 17, 517-521.

P.L. Hooper, P.L. Hooper, M. Tytell, L. Vígh (2010) Xenohormesis: Health benefits from an eon of plant stress response evolution, Cell Stress and Chaperones, 15(6), 761-770.

P.L. Hooper and P.L. Hooper (2009) Inflammation, heat shock proteins, and type 2 diabetes, Cell Stress and Chaperones 14(2), 113-115.

J. Chung, A. Nguyen, D.C. Henstridge, A.G. Holmes, M.H. Stanley Chan, J.L. Mesa, G.I. Lancaster, R.J. Southgate, C.R. Bruce, S.J. Duffy, I. Horvath, R. Mestril, M.J. Watt, P.L. Hooper, B.A. Kingwell, L. Vigh, A. Hevener, and M.A. Febbraio (2008) HSP72 protects against obesity-induced insulin resistance PNAS 105(5), 1739-1744. [Also highlighted in Nature Medicine.]

P.L. Hooper (2007) Insulin signaling, GSK-3, heat shock proteins and the natural history of type 2 diabetes mellitus: A hypothesis, Metabolic Syndrome and Related Disorders 5(3), 220-230.

P.L. Hooper and J.J. Hooper (2005) Loss of defense against stress: Diabetes and heat shock proteins, Diabetes Technology and Therapeutics 7(1), 204-208.

P.L. Hooper (2005) Systemic diabetes mellitus, Diabetes Technology and Therapeutics 7(2), 337.

P.L. Hooper and J.J. Hooper (2004) Is low-heat shock protein 70 a primary or a secondary event in the development of atherosclerosis? Hypertension 43(4), 18-19.

P.L. Hooper and J.J. Hooper (2004) Vitamin E, atherosclerosis, heat shock proteins: The Trojan Horse hypothesis, Preventive Cardiology 7(3), 144.

P.L. Hooper (2003) Diabetes, nitric oxide, and heat shock proteins, Diabetes Care 26(3), 951.

M. Tytell and P.L. Hooper (2001) Heat shock proteins: New keys to the development of cytoprotective therapies, Emerging Theraputic Targets 5(2), 267-287.

P.L. Hooper (2001) Reduced heat shock proteins: A mechanism to explain higher cardiovascular events associated with doxazosin, Journal of Human Hypertensions 15, 213.

P.L. Hooper (2001) Hypothesis to explain poor outcomes in the ALLHAT and V-HeFT trials: Decreased expression of heat shock proteins, Current Controlled Trials in Cardiovascular Medicine 2(6), 251-253.

P.L. Hooper (1999) Hot-tub therapy for type 2 diabetes mellitus, New England Journal of Medicine 341(12), 924-925.


Curriculum vitae