Dr. Michael J. Quon completed his undergraduate education in Biomedical Engineering at Northwestern University in 1982. Subsequently, he obtained both a Ph.D. in Biomedical Engineering (1987) as well as an M.D. (1988) from Northwestern University. After a residency in Internal Medicine at the University of Chicago (1988-90), Dr. Quon completed subspecialty training in Diabetes, Endocrinology and Metabolism (1990-93) at the National Institutes of Health (NIH). During this time, Dr. Quon also received post-doctoral training in molecular biology in the laboratory of Dr. Simeon I. Taylor (1991-1995). From 1995-2001, Dr. Quon was a tenure-track Investigator in the Hypertension-Endocrine Branch of the National Heart, Lung, and Blood Institute at NIH where he established a productive independent laboratory that studied molecular mechanism of insulin action and insulin resistance as they relate to diabetes, obesity, and cardiovascular diseases. Dr. Quon also performed patient-oriented clinical studies to understand the physiology of glucose metabolism and the hemodynamic actions of insulin in humans. In addition, he used mathematical modeling at both the molecular and whole body level to gain additional insights into insulin action. In 2002, Dr. Quon was appointed as a tenured Senior Investigator and Chief of the Diabetes Unit in the National Center for Complementary and Alternative Medicine at NIH where he continued his laboratory and clinical studies on insulin action and insulin resistance. In particular, Dr. Quon elucidated mechanisms for nutritional supplements and functional foods to either improve or impair metabolic and vascular actions of insulin using molecular, cellular, physiological, mathematical, and clinical research approaches. Dr. Quon joined the University of Maryland School of Medicine in 2011.
Dr. Quon currently serves as Associate Editor for the American Journal of Physiology: Endocrinology and Metabolism and is Editor-in-Chief of Reviews in Endocrine and Metabolic Disorders. Dr. Quon received the NIH Director's Award for Mentoring in 2004 and he is the recipient of numerous Mentor and Research Awards from the American Diabetes Association. He is an elected Fellow of the Council for High Blood Pressure Research and the American Heart Association. Dr. Quon has published over 195 peer-reviewed papers in leading medical and scientific journals that have been cited >19,500 times in the scientific literature. Dr. Quon has an H-index of 69 and he is regularly invited to speak at national and international scientific meetings.
The overarching goal of our lab is to understand molecular mechanisms of insulin action, insulin resistance, and endothelial dysfunction as they relate to diabetes, obesity and their cardiovascular complications. We employ approaches spanning molecular and cellular biology, physiology, mathematical modeling, and patient-oriented clinical investigation. One major hypothesis our lab pioneered is that insulin-stimulated production of nitric oxide (NO) in vascular endothelium functions to couple metabolic and vascular physiology. This also determines, in part, reciprocal relationships between insulin resistance and endothelial dysfunction. A second important hypothesis is that imbalance between PI 3-kinase- and MAP-kinase-dependent insulin signaling pathways caused by insulin resistance contributes to coupling of vascular and metabolic pathophysiology. Corollaries include the idea that therapeutic strategies to improve metabolic actions of insulin will simultaneously improve endothelial function and vice versa. We have made substantial contributions in four broad areas related to insulin action that are mutually informative and that help to explain mechanisms linking genetic disorders including diabetes, obesity, and their cardiovascular complications: 1) metabolic actions of insulin, 2) complexity in insulin signaling, 3) vascular actions of insulin, and 4) clinical physiology of insulin's metabolic and vascular actions.
- Internal Medicine
Lab Techniques and Equipment:
- Molecular Biology, Cellular Biology, Animal Physiology, Patient-oriented Clinical Research
- Glucose clamp
- Vascular ultrasound studies of brachial artery and capillary recruitment
- Forearm plethysmography
- Primary adipose cells
- Primary endothelial cells
Selected Publications from over 180
Zeng, G., Quon, M.J.: Insulin-stimulated production of nitric oxide is inhibited by wortmannin: direct measurement in vascular endothelial cells. J. Clin. Invest. 98:894-898, 1996. (Rapid Publication).
Katz, A., Nambi, S., Mather, K., Baron, A.D., Follman, D.A., Sullivan, G., Quon, M.J.: Quantitative insulin-sensitivity check index (QUICKI): a simple, accurate method for assessing insulin sensitivity in vivo. J. Clin. Endocrinol. Metab. 85:2402-2410, 2000.
Montagnani, M., Chen, H., Barr, V.A., Quon, M.J.: Insulin-stimulated activation of eNOS is independent of Ca++ but requires phosphorylation by Akt at Ser1179. J. Biol. Chem. 276:30392-30398, 2001.
Chen, H., Montagnani, M., Funahashi, T., Shimomura, I., Quon, M.J.: Adiponectin stimulates production of nitric oxide in vascular endothelial cells. J. Biol. Chem. 278:45021-45026, 2003.
Koh, K.K., Quon, M.J., Chung, W.J., Han, S.H., Ahn, J.Y., Seo, Y.H., Kang, W.C., Kang, M.H., Ahn, T.H., Choi, I.S., Shin, E.K.: Additive beneficial effects of losartan combined with simvastatin in the treatment of hypercholesterolemic, hypertensive patients. Circulation 110:3687-3692, 2004.
Kim, J., Yeh, D.C., Ver, M., Li, Y., Carranza, M.A., Conrads, T.P., Veenstra, T.D., Harrington, M., Quon, M.J.: Phosphorylation of Ser24 in the PH domain of IRS-1 by mPLK/IRAK: cross-talk between inflammatory signaling and insulin siganling that may contribute to insulin resistance. J. Biol. Chem. 280:23173-23183, 2005.
Kim, J., Montagnani, M., Koh, K.K., Quon, M.J.: Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms. Circulation 113:1888-1904, 2006.
Kim, J., Formoso, G., Li, Y., Potenza, M.A., Marasciulo, F.L., Montangnani, M., Quon, M.J.: Epigallocatechin gallate, a green tea polyphenol, mediates NO-dependent vasodilation using signaling pathways in vascular endothelium requiring reactive oxygen species and Fyn. J. Biol. Chem. 282:13736-13745, 2007.
Muniyappa, R., Montagnani, M., Koh, K.K., Quon, M.J.: Cardiovascular actions of insulin. Endocrine Reviews, 28:463-491, 2007.
Muniyappa, R., Lee, S., Chen, H., Quon, M.J.: Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am. J. Physiol. Endocrinol. Metab. 294:E15-E26, 2008.
Chen, H., Lin, A.S., Li, Y., Reiter, C., Ver, M.R., Quon, M.J.: DHEA stimulates phosphorylation of FoxO1 in vascular endothelial cells via PI3-kinase- and PKA-dependent signaling pathways to regulate ET-1 synthesis and secretion. J. Biol. Chem. 283:29228-29238, 2008.
Reiter, C.E.N., Kim, J., Quon, M.J.: Epigallocatechin gallate, a green tea polyphenol, reduces endothelin-1 expression in vascular endothelial cells through FOXO1-dependent transcriptional regulation. Endocrinology 151:103-114, 2010.
Lee, J.W., Chen, H., Pullikotil, P., Quon, M.J.: Protein Kinase A-Î± directly phosphorylates FoxO1 in vascular endothelial cells to regulate activity of VCAM-1. J. Biol. Chem. 286:6432-6423, 2011.
Rizza, S., Muniyappa, R., Iantorno, M., Kim, J., Chen, H., Pullikotil, P., Senese, Nicoletta, Tesauro, M., Lauro, D., Cardillo, C., Quon, M.J.: The citrus polyphenol hesperedin stimulates production of nitric oxide in endothelial cells to improve endothelial function and reduce inflammatory markers in patients with metabolic syndrome.J. Clin. Endocrinol. Metab. , 96:E782-92, 2011.
Munir, K.M., Quon, M.J.: Distinc mechanisms for globular adiponectin that integrate vascular and metabolic actions of insulin to help maintain coordinated cardiovascular and glucose homeostasis. Circ. Res. 112:1205 - 7, 2013.
Munir, K.M., Quon, M.J.: Mechanisms for food polyphenols to ameliorate insulin resistance and endothelial dysfunction: therapeutic implications for diabetes and its vascular complications. Am. J. Physiol. Endocrinol. Metab. 305:E679-E686, 2013.
Koh, K.K., Lim, S., Choi, H., Lee, Y., Han, S., Lee, K., Oh, P., Sachiro, I., Shin, E., Quon, M.J.: Combination pravastatin and valsartan treatment have additive beneficial effects to simultaneously improve both metabolic and cardiovascular phenotypes beyond that of monotherapy with either drug in patients with primary hypercholesterolemia. Diabetes 62:3547-3552, 2013.
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