Obesity and diabetes are epidemic. They account for substantial morbidity, mortality and costs. Novel strategies to prevent and treat diabetes and its complications are desperately needed. By targeting the pathophysiology of obesity-related diabetes and performing preclinical and clinical studies in parallel, we hope to accelerate the discovery of new targets for therapies. Sanford-Burnham, in collaboration Florida Hospital and the Translational Research Institute for Metabolism and Diabetes, provide unparalleled opportunities for advancing new discoveries into the clinic.
Dr. Pratley focuses on the role of adipose tissue and adipocyte secreted products in the pathogenesis of type 2 diabetes.
Dr. Pratley received his M.D. from Wayne State University, Detroit, MI.
Sexually dimorphic diet-induced insulin resistance in obese tissue inhibitor of metalloproteinase-2 (TIMP-2)-deficient mice.
Jaworski DM, Sideleva O, Stradecki HM, Langlois GD, Habibovic A, Satish B, Tharp WG, Lausier J, Larock K, Jetton TL, Peshavaria M, Pratley RE
Endocrinology. 2011 Apr;152(4):1300-13
Liraglutide versus sitagliptin for patients with type 2 diabetes who did not have adequate glycaemic control with metformin: a 26-week, randomised, parallel-group, open-label trial.
Pratley RE, Nauck M, Bailey T, Montanya E, Cuddihy R, Filetti S, Thomsen AB, Søndergaard RE, Davies M, 1860-LIRA-DPP-4 Study Group
Lancet. 2010 Apr 24;375(9724):1447-56
Plasma amyloid-beta peptide levels correlate with adipocyte amyloid precursor protein gene expression in obese individuals.
Lee YH, Martin JM, Maple RL, Tharp WG, Pratley RE
Treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin improves fasting islet-cell function in subjects with type 2 diabetes.
D'Alessio DA, Denney AM, Hermiller LM, Prigeon RL, Martin JM, Tharp WG, Saylan ML, He Y, Dunning BE, Foley JE, Pratley RE
J Clin Endocrinol Metab. 2009 Jan;94(1):81-8
The cannabinoid CB1 receptor is expressed in pancreatic delta-cells.
Tharp WG, Lee YH, Maple RL, Pratley RE
Biochem Biophys Res Commun. 2008 Aug 8;372(4):595-600
Amyloid precursor protein expression is upregulated in adipocytes in obesity.
Lee YH, Tharp WG, Maple RL, Nair S, Permana PA, Pratley RE
Obesity (Silver Spring). 2008 Jul;16(7):1493-500
Microarray profiling of skeletal muscle tissues from equally obese, non-diabetic insulin-sensitive and insulin-resistant Pima Indians.
Yang X, Pratley RE, Tokraks S, Bogardus C, Permana PA
Diabetologia. 2002 Nov;45(11):1584-93
Subcutaneous abdominal adipocyte size, a predictor of type 2 diabetes, is linked to chromosome 1q21--q23 and is associated with a common polymorphism in LMNA in Pima Indians.
Weyer C, Wolford JK, Hanson RL, Foley JE, Tataranni PA, Bogardus C, Pratley RE
Mol Genet Metab. 2001 Mar;72(3):231-8
Effects of an Ala54Thr polymorphism in the intestinal fatty acid-binding protein on responses to dietary fat in humans.
Pratley RE, Baier L, Pan DA, Salbe AD, Storlien L, Ravussin E, Bogardus C
J Lipid Res. 2000 Dec;41(12):2002-8
The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus.
Weyer C, Bogardus C, Mott DM, Pratley RE
J Clin Invest. 1999 Sep;104(6):787-94
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Pioglitazone Prevents Diabetes in Insulin-Resistant Patients With Cerebrovascular Disease.
Inzucchi SE, Viscoli CM, Young LH, Furie KL, Gorman M, Lovejoy AM, Dagogo-Jack S, Ismail-Beigi F, Korytkowski MT, Pratley RE, Schwartz GG, Kernan WN, IRIS Trial Investigators
Diabetes Care. 2016 Jul 27;
Richard Pratley's Research Focus
Aging-Related Diseases, Metabolic Syndrome, Monogenic Diabetes, Diabetes - General, Type 1 Diabetes, Type 2 Diabetes, Alzheimer's Disease
The aims of the Pratley lab are to:
1. Understand the role adipocyte proliferation and differentiation play in the pathogenesis of insulin resistance and type 2 diabetes.
2. Understand how glucose-dependent insulinotropic peptide (GIP) signaling is altered in obesity and type 2 diabetes and how this contributes to metabolic dysfunction.
3. Understand the mechanisms leading to dysregulation of amyloid precursor protein (APP) and its cleavage products in obesity and type 2 diabetes and how this contributes to inflammation and metabolic dysfunction.
About Richard Pratley
Richard E. Pratley, M.D., is a graduate of Wayne State University School of Medicine in Detroit, Michigan, and trained in internal medicine at the University of Michigan in Ann Arbor. He served as Head of the Diabetes and Metabolism Unit of the National Institutes of Health Clinical Diabetes and Nutrition Section in Phoenix, Arizona, before taking a position as Senior Director in the Cardiovascular and Metabolism Therapeutic Area at Novartis Pharmaceuticals, where he worked on the clinical development of new drugs for diabetes until 2004.
From 2004-2011, Dr. Pratley was Professor of Medicine, University of Vermont College of Medicine and Director of the Diabetes and Metabolism Translational Medicine Unit. His current research interests include the prevention of diabetes, improving the care for persons with diabetes, developing new drugs to treat and prevent diabetes and its complications, and understanding the role of the fat cell in increasing the risk for diabetes and heart disease.
M.D., Wayne State University, Detroit, MI
B.S. with Honors, Cell and Molecular Biology, University of Michigan, Ann Arbor, MI
Director, Florida Hospital Diabetes Institute
Senior Scientist, Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes
Honors and Recognition
Best paper published in the journal Obesity, 2009
Henry Christian Award for Excellence in Clinical Research, American Federation for Clinical Research, 1992