Ronald L Prigeon M.D.

Academic Title: Assistant Professor
Primary Appointment: Medicine
Secondary Appointments: Medicine
rprigeon@grecc.umaryland.edu
Location: Baltimore VA Medical Center, Room 4B-191
Phone: (410) 605-5422
Fax: (410) 605-7913

Research Interests

Dr. Prigeon's research emphasis is on the physiology and pathophysiology of type-2 diabetes. Maintenance of normal glucose homeostasis requires a balance between insulin production from the pancreatic beta cell and insulin sensitivity. For example, if a person develops the insulin resistance syndrome, the insulin output from the beta cell must increase in order to maintain normal glucose tolerance and failure of this adaptive mechanism will result in impaired glucose tolerance or frank diabetes. The specific areas of research activity include examining beta cell adaptation to insulin resistance in normal young and old subjects and in subjects at increased risk of developing diabetes such as obese individuals. In connection with this research, two additional areas of interest are the mathematical modeling of physiological systems (with and without the use of tracers) and development of techniques for the measurement of beta cell function and insulin sensitivity. Trainees will gain exposure to research in whole-body physiology and will be exposed to various techniques for measuring insulin sensitivity and beta cell function such as the minimal model, clamp techniques, graded glucose infusions and insulin response to non-glucose secreatagogues.

Publications

Most Recent Publications
Hull RL, Kodama K, Utzschneider KM, Carr DB, Prigeon RL, Kahn SE: Dietary-fat-induced obesity in mice results in beta cell hyperplasia but not increased insulin release: evidence for specificity of impaired beta cell adaptation. Diabetologia 48:1350-1358 2005.

D'Alessio DA, Vahl TP, Prigeon RL. Effects of glucagon-like peptide 1 on hepatic glucose metabolism. Horm Metab Res  36:837-841 2004.

Hull RL, Andrikopoulos S, Verchere CB, Vidal J, Wang F, Cnop M, Prigeon RL, Kahn SE: Increased Dietary Fat Promotes Islet Amyloid Formation and ß-cell Secretory Dysfunction in a Transgenic Mouse Model of Islet Amyloid. Diabetes 52:372-379 2003.

Quddusi S, Vahl TP, Hanson K, Prigeon RL, D'Alessio DA. Differential effects of acute and extended infusions of Glucagon like peptide-1 (GLP-1) on first and second phase insulin secretion in diabetic and nondiabetic humans. Diabetes Care 26:791-798 2003.

Vahl TP, Paty BW, Fuller BD, Prigeon RL, D'Alessio DA. Effects of GLP-1[7-36]NH2, GLP-1[7-37] and GLP-1[9-36]NH2 on intravenous glucose tolerance and glucose-induced insulin secretion in healthy humans. J Clin Endocrinol Metab 88:1772-1779 2003.

Prigeon RL, Quddusi S, Paty BW, D'Alessio DA. Suppression of endogenous glucose production by glucagon-like peptide 1 independent of islet hormones: An extrapancreatic effect of an incretin hormone. Am J Physiol 285:E701-707 2003.

Greenbaum CJ, Prigeon RL, D'Alessio DA. Impaired ß-Cell Function, Incretin Effect and Glucagon Suppression in Patients With Type 1 Diabetes Who Have Normal Fasting Glucose. Diabetes 51: 951-957 2002.

Kahn SE, Prigeon RL, Schwartz RS, Fujimoto WY, Knopp RH, Brunzell JD, Porte D Jr. Obesity, body fat distribution, insulin sensitivity and islet cell function as explanations for metabolic diversity. J Nutr 131:354S-360S 2001.

Roder ME, Schwartz RS, Prigeon RL, Kahn SE. Reduced pancreatic B-cell compensation to the insulin resistance of aging: Impact on proinsulin and insulin levels. J Clin Endocrinol Metab 85:2275-2280 2000.

Verchere CB, D'Alessio DA, Prigeon RL, Hull RL, Kahn SE. The constitutive secretory pathway is a major route for islet amyloid polypeptide secretion in neonatal but not adult rat islet cells. Diabetes 49:1477-1484 2000.

Kaiyala KJ, Prigeon RL, Kahn SE, Woods SC, Schwartz MW. Obesity induced by a high-fat diet is associated with reduced brain insulin transport in dogs. Diabetes 49:1525-1533 2000.




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