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Faculty Detail     Name JEONGA KIM   Campus Address BDB 777 Zip 0012 Phone 205-934-4116 E-mail jakim@uab.edu Other websites

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Medicine  Med - Endocrinology, Diabetes & Metabolism Assistant Professor Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Assistant Professor Center  Medicine  Comprehensive Diabetes Ctr Assistant Professor Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Assistant Professor

Biographical Sketch  Education 1984 BS : Food and Nutrition, Yonsei University, Seoul, Korea 1986 MS : Biochemistry, Yonsei University, Seoul, Korea 1997 PhD: Genetics, Iowa State University Post-Doctoral Training 1997-1999: Pennsylvania State University, College of Medicine, Cellular and Molecular Physiology Dept. 2002-2007: Diabetes Unit, NCCAM, NIH Awards and Honors 1996 and 1997 Stadler Fellowship by the Interdepartmental Genetics Major, Iowa State University 2004 and 2006 NIH FARE Award for Research Excellence 2004 American Diabetes Association Travel Grant

Society Memberships Organization Name Position Held Org Link American Diabetes Association    http://www.diabetes.org/  American Heart Association    http://www.americanheart.org/presenter.jhtml?identifier=1200000

Research/Clinical Interest Title Cross-talk between inflammation and insulin signaling Description Insulin resistance is centered in the pathogenesis of cardiometabolic syndrome. My current research focuses on understanding the mechanisms of insulin resistance and endothelial dysfunction caused by pro-inflammatory signaling. This includes identification and characterization of specific kinases that impair insulin signaling in both metabolic and cardiovascular tissues. In related studies, I am investigating mechanisms for bioactive polyphenols to ameliorate cardiovascular and metabolic diseases. Cross-talk between inflammation and insulin signaling – Obesity, insulin resistance, dyslipidemia, and hypertension cluster together in the metabolic syndrome. Inflammatory signaling pathways activate various kinases that impair insulin signaling resulting in insulin resistance. My first project is focused on investigating the signaling pathways that are activated by high fat diet, which leads to stimulation of inflammatory signaling. One hypothesis regarding fatty acid-induced inflammatory signaling is that production of reactive oxygen species leads to activation of IKK. Recently, it has been reported that free fatty acids specifically activate Toll-like receptors. The activation of Toll-like receptors is involved in high fat diet induced insulin resistance and cardiovascular diseases. However, the detailed mechanism between toll-like receptor and dietary fat is not clearly understood. I plan to elucidate molecular mechanisms for fatty acids to activate toll-like receptors and related signal transduction pathways. In addition, I plan to investigate the regulation of genes by fatty acid stimulation through toll-like receptors. The results of this project will help us to understand the molecular mechanisms underlying high fat diet induced insulin resistance and endothelial dysfunction. Polyphenolic compounds that ameliorate insulin resistance and endothelial dysfunction – Polyphenols in green tea (EGCG), red wine (resveratrol), citrus fruit (naringenin), and chocolate (epicatechin) have vasodilator actions that may ameliorate hypertension and insulin resistance. I have been studying the biological actions of EGCG, especially with regard to endothelial function. We found that EGCG activates eNOS and NO production through a Fyn dependent mechanism. We also observed that hesperetin and naringenin to promote vasodilation and anti-inflammatory effects through activation of PI 3-kinase/Akt, and/or AMPK/eNOS/NO pathways. In related studies, I would like to examine whether various polyphenolic compounds can inhibit inflammatory signaling pathways and improve fatty acid-induced insulin resistance. These studies may give additional novel insights related to molecular mechanisms for insulin resistance and endothelial dysfunction. Linking inflammation with the metabolic syndrome is highly relevant to major public health problems. The results of these projects may contribute to prevention and treatment of cardiovascular and metabolic diseases.

Selected Publications  Publication PUBMEDID 1. JA Kim, JE Mayfield. Brucella abortus arginase and ornithine cyclodeaminase genes are similar to Ti plasmid arginase and ornithine cyclodeaminase. Biochim Biophys Acta (1997) 1354, 55-57. 2. JA Kim, Z Sha, JE Mayfield. Brucella abortus periplasmic catalase is regulated in response to external H2O2. Infect Immun (2000) 68, 3861-3866 3. JA Kim, JE Mayfield. Identification of Brucella abortus OxyR and its Role in Control of Catalase Expression. J Bacteriol (2000) 182, 5631-5633 4. JA Kim, J Lu, PG Quinn: Distinct CREB domains stimulate different steps in a concerted mechanism of transcription activation. Proc Natl Acad Sci USA (2000) 97, 11292-11296 5. EA Felinski, JA Kim, J Lu, PG Quinn: Recruitment of an RNA polymerase II complex is mediated by the constitutive activation domain in CREB, independently of CREB phosphorylation. Mol. Cell. Biol. (2001) 21, 1001-1010 6. DH Kim, JA Kim, JS Choi, CK Joo: Activation of caspase-3 during degeneration of ONL in rd mouse retina. Ophthalmic Res (2002) 34, 150-157 7. MJ Lee, SS Cho, JR You, Y Lee, BD Kang, JS Choi, JW Park, YL Suh, JA Kim, D-K Kim, J-S Park: Intraperitoneal gene delivery mediated by a novel cationic liposome in a peritoneal disseminated ovarian cancer model. Gene Ther (2002) 9, 859-866 8. HS Jang, HJ Kim, JM Kim, YS Lee, KL Kim, JA Kim, JY Lee, W Suh, JH Choi, ES Jeon, J Byun, DK Kim: A novel ex vivo angiogenesis assay based on electroporation-mediated delivery of naked plasmid DNA to skeletal muscle: Mol Ther. (2004) 9, 464-74 9. JA Kim, DC Yeh, M Ver, Y Li, A Carranza, TP Conrads, TD Veenstra, MA Harrington, MJ Quon: Phosphorylation of Ser24 in the PH domain of IRS-1 by mPLK/IRAK: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. J Biol Chem. (2005) 280, 23173-83 10. JA Kim, KK Koh, MJ Quon: The union of vascular and metabolic actions of insulin in sickness and in health. Arterioscler Thromb Vasc Biol. (2005) 25, 889-91 11. KK Koh, MJ Quon, SH Han, WJ Chung, JY Ahn, JA Kim, Y Lee, EK Shin: Additive beneficial effects of fenofibrate combined with candesartan in the treatment of hypertriglyceridemic, hypertensive patients. Diabetes Care, (2006) 29, 195-201 12. G Formoso, H Chen, JA Kim, M Montagnani, A Consoli, MJ Quon: DHEA mimics acute actions of insulin to stimulate production of both NO and ET-1 via distinct PI 3-kinase- and MAP-kinase- dependent pathways in vascular endothelium Mol Endocrinol. (2006) 20, 1153-1163 13. JA Kim, M Montagnani, KK Koh, MJ Quon: Reciprocal Relationships Between Insulin Resistance and Endothelial Dysfunction: molecular and pathophysiological mechanisms Circulation (2006) 113, 1888-904 14. KK Koh, MJ Quon, SH Han, WJ Chung, JA Kim, EK Shin: Vascular and metabolic effects of candesartan: insights from therapeutic interventions. J. Hypertens Suppl. (2006), 24, S31-8. 15. MW Greene, MS Ruhoff, RA Roth, JA Kim, MJ Quon, JA Krause: PKC- mediated IRS-1 Ser24 phosphorylation negatively regulates IRS-1 function. : Biochem Biophys Res Commun (2006) 349, 976-986. 16. M Iantorno, H Chen, JA Kim, M Tesauro, D Lauro, C Cardillo, MJ Quon: Ghrelin has Novel Vascular Actions that Mimic Only PI 3-kinase-dependent Insulin-stimulated Production of Nitric Oxide (NO) but Not MAP-kinase-dependent Insulin-stimulated Secretion of ET-1 From Endothelial Cells. Am J Physiol Endocrinol Metab (2007) 292, 756-764. 17. MA Potenza, FL Marasciulo, M Tarquinio, E Tiravanti, G Colantuono, A Federici, JA Kim, MJ Quon, and M Montagnani: Epigallocatechin Gallate (EGCG), a Green Tea Polyphenol, Reduces Blood Pressure, Improves Insulin sensitivity, and Protects Against Myocardial Ischemia/Reperfusion (I/R) Injury in Spontaneously Hypertensive Rats (SHR). :Am J Physiol Endocrinol Metab (2007) 292,1378-1387 18. JA Kim, M Montangnani, G Formoso, Y Li, and MJ Quon: Epigallocatechin gallate (EGCG), agreentea polyphenol, mediates NO-dependent vasodilation using signaling pathway in vascular endothelium involving Fyn, PI 3-kinase, Akt, and eNOS : J Biol Chem (2007) 282,13736-13745. 19. KK Koh, MJ Quon, SJ Lee, SH Han, JY Ahn, JA Kim, Y Lee, E.K Shin: Efonidipine simultaneously improves blood pressure, endothelial function, and metabolic parameters in nondiabetic patients with hypertension. Diabetes care, (2007) 30,1605-1607 20. KK Koh, MJ Quon, SH Han, JY Ahn, JA Kim, Y Lee, EK Shin: Additive beneficial cardiovascular and metabolic effects of combination therapy with ramipril and cardesartan in hypertensive patients. Eur Heart J. (2007) 28,1440-1447. 21. S Lee, EG Lynn, JA Kim, MJ Quon: Protein kinase C-{zeta} phosphorylates insulin receptor substrate-1, -3, and -4, but not -2: isoform specific determinants of specificity in insulin signaling. Endocrinology, (2008) 149, 2451-8. 22. JA Kim, Y Wei, JR Sowers: Role of mitochondrial dysfunction in insulin resistance: Cir. Res, (2008) 29, 401-14. 23. JA Kim: Mechanisms underlying beneficial health effects of tea catechins to improve insulin resistance and endothelial dysfunction: Endocrine, Metabolic & Immune Disorders - Drug Targets (2008) 8, 82-88 24. CE Reiter, JA Kim, MJ Quon: The green tea polyphenol EGCG reduces ET-1 expression and secretion in vascular endothelial cells: roles for AMPK, Akt, and FOXO1: Endocrinology (2010) 151(1), 103-14 25. X Zhou, L Ma, J Habibi, A Whaley-Connell, MR Haydon, RD Tilmon, AN Brown, JA Kim, VG Demarco, Sowers JR: Nebivolol Improves Diastolic Dysfunction and Myocardial Remodeling Through Reductions in Oxidative Stress in the Zucker Obese Rat: Hypertension (2010) published on line Feb 22, 2010

Keywords Insulin Resistance, Endothelial Dysfunction, NO, ROS, Polyphenol

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