Norman Fleischer is the Barkey Professor of Medicine, Director of Endocrinology, and Co-Director of the Diabetes Research Center of the Montefiore Medical Center and Albert Einstein College of Medicine. A graduate of the Vanderbilt University School of Medicine, he completed his residency in Medicine at Jacobi Medical Center, and his Fellowship in Endocrinology at Vanderbilt University under the mentorship of Grant W. Liddle, M.D. He then joined the faculty of Baylor College of Medicine in Houston, Texas, where he served as Chief of Endocrinology at Ben Taub General Hospital. In 1973, he joined the faculty at Albert Einstein College of Medicine.
In 1976, he was appointed Director of the Division of Endocrinology at Einstein, and in 1977 became the founding Director of the NIH-funded Diabetes Research and Training Center. In 1988, Dr. Fleischer was appointed Director of the Diabetes Research Center of the Albert Einstein College of Medicine, a quasi-departmental University based center. In 1999, he was also appointed Director of Endocrinology of Montefiore Medical Center. Dr. Fleischer continues an active career in clinical endocrinology, research, and administration, with continuous involvement in the educational programs for students, residents, and especially, endocrine fellows.
His research has been on the regulation of polypeptide hormone production and secretion, especially that of insulin. He has studied the mechanisms involved in glucose, fatty acid, and incretin-mediated insulin secretion. For these studies he utilized conditionally transformed murine beta cell lines in which replication is controllable. These cells have also been studied by Dr. Fleischer as model systems for beta cell transplantation to treat diabetes.
Erlichman, J., Litvin, Y., and Fleischer, N.:Immunological and Molecular Characterization of cAMP‑dependent Protein Kinases in AtT‑20 cells. J. Biol. Chem. 259: 10289‑10295, 1984.
Leiser, M., Fleischer, N. and Erlichman, J.: Enhanced Activation of cAMP-dependent Protein Kinase by Rapid Synthesis and Degradation of cAMP. J. Biol. Chem. 261: 15486-15490, 1986.
Bilezikjian, L.M., Erlichman, J., Fleischer, N. and Vale, W.W.: Differential activation of type I and type II cAMP-dependent protein kinases by growth hormone releasing factor. Molecular Endocrinology 1: 137-146, 1987.
Fleischer, N., Liker, H., Stoller, T., and Shields, D.: Retrovirus-Mediated Expression of Preprosomatostatin in Rat Pituitary GH3 Cells: Targeting of somatostatin to the regulated secretory pathway. Molecular Endocrinology. 3:1652-1658, 1989.
Lomasky, S.J., D'Eramo, G., Shamoon, H. and Fleischer, N.: Relation of Insulin Secretion and Glycemic Recovery to Dietary Intervention in Non-Insulin-Dependent Diabetes. Arch. Intern. Med. 150:169-172, 1990.
Efrat, S., Fleischer, N., and Hanahan, D.: Diabetes Induced in Male Transgenic Mice by Expression of Human H-ras Oncoprotein in Pancreatic Beta Cells. Mol. Cell. Biol. 10: 1779-1783, 1990.
D'Ambra, R.D., Surana, M., Efrat, S., Starr, R.G., and Fleischer, N.: Regulation of Insulin Secretion from Beta Cell Lines Derived from Transgenic Mice Insulinomas Resembles That of Normal Beta Cells. Endocrinology 126: 2815-2822, 1990.
Efrat, S., Surana, M., and Fleischer, N.: Glucose induces insulin gene transcription in a murine Beta-cell line. J. Biol. Chem., 266:11141-11143, 1991.
Tal, M., Wu, Y-J, Leiser, M., Surana, S., Lodish, H., Fleischer, N., Weir, G., and Efrat, S.: [Val12]HRAS downregulates GLUT2 in cells of transgenic mice without affecting glucose homeostasis. Proc. Natl. Acad. Sci. USA, 89:5744-5748, 1992.
Efrat, S., Leiser, M., Surana, M., Tal, M., Fusco-DeMane, D., and Fleischer, N.: A murine insulinoma cell line with normal glucose-regulated insulin secretion. Diabetes 42:901-907, 1993
Efrat, S., Leiser, M., Wu, Y-J., Fusco-DeMane, D., Emran, O., Surana. M., Weir, G., Jetton, T., Magnuson, M.A., and Fleischer, N.: Ribozyme-mediated attenuation of pancreatic-cell glucokinase expression in transgenic mice results in impaired glucose-induced insulin secretion. Proc. Natl. Acad. Sci (USA), 91:2051-2055, 1994.
Knaack, D., Fiore, D.M., Surana, M., Leiser, M., Laurance, M., Fusco-DeMane, D., Fleischer, N., and Efrat, S.: Clonal insulinoma cell line which maintains correct glucose responsiveness. Diabetes 43:1413-1417, 1994
Leiser, M., Efrat, S., and Fleischer, N.: Evidence that RAP1 carboxylmethylation is involved in regulated insulin secretion. Endocrinology 136: 2521-2530, 1995.
Bali, D., Svetlanov, A., Lee, H., Fusco-DeMane, D., Leiser, M., Li, B., Barzilai, N., Surana, M., Hou, H., Fleischer, N., DePinho, R., Rossetti, L., and Efrat, S.: Animal model for maturity-onset diabetes of the young generated by disruption of the mouse glucokinase gene. J. Biol. Chem. 270:21464-21467, 1995.
Leiser, M., and Fleischer, N., cAMP-Dependent Phosphorylation of the Cardiac-type a1 Subunit of the Voltage-dependent Ca++Channel in a Murine Pancreatic-Cell Line. Diabetes 45:1412-1418, 1996.
Fleischer, N., Chen, C., Surana, M., Leiser, M., Rossetti, L., Pralong, W., and Efrat, S., Functional Analysis of a Conditionally-Transformed Pancreatic-Cell Line. Diabetes 47:1419-1425, 1998.
Han P, Werber J, Surana M, Fleischer N and Michaeli T:The calcium calmodulin dependent phosphodiesterase PDE1C down‑regulates glucose induced insulin secretion. J. Biol. Chem. 274:22337‑44, 1999.
Sooy K, Schermerhorn T, Noda M, Rhoten WB, Meyer M, Fleischer N, Sharp GWG, Christakos S: Calbindin-D28k controls [Ca2+]iand insulin release: evidence obtained from calbindin-D28k knockout mice and cell lines. J.Biol. Chem., 274:34343-49, 1999.
Efrat S, and Fleischer N: Engineering the pancreatic-cell. In Diabetes Mellitus (D. LeRoith, S. Taylor, J. Olefsky, eds.) Lippincott-Raven, Philadelphia, p535-541, 2000
Cases, JA, Gabriely I, Xiao HM, Xiao MY, Michaeli T, Fleischer N, Rossetti L, Barzilai N: Physiological increase in plasma leptin markedly inhibits insulin secretion in vivo. Diabetes 50:348-352, 2001.
Milo-Landesman D, Surana M, Berkovich I, Compagni A, Christofori G, Fleischer N and Efrat S: Correction of hyperglycemia in diabetic mice transplanted with reversibly-immortalized pancreatic b cells controlled by the tet-on regulatory system. Cell Transplantation 10:645-659 (2001).
Zalzman M, Gupta S, Giri RK, Berkovich I, Sappal BJ, Karnieli O, Zern MA, Fleischer N, and Efrat S. Reversal of hyperglycemia in mice using human expandable insulin-producing cells differentiated from fetal liver progenitor cells; Proc. Natl. Acad. Sci.(USA), 100:7253-7258, 2003
Howard A, Floris-Moore M, Arnsten J, Santoro N, Fleischer N, Lo Yungtai, Schoenbaum E, Disorders of Glucose Metabolism among HIV-Infected Women Clinical Infectious Diseases 2005; 40:1491-9
Howard A, Floris-Moore M. Lo Y, Arnsten JH, Fleischer N, Klein RS, Abnormal glucose metabolism among older men with or at risk of HIV infection; 2006 British HIV Association; HIV Medicine (2006), 7, 389-396
T. Kojaoghlanian, A. Joseph, A. Follenzi, J. H. Zheng, M. Leiser, N. Fleischer, M. M. S.. Horwitz, T. P. DiLorenzo, and H. Goldstein. Lentivectors Encoding Immunosuppressive Proteins Genetically Engineer Pancreatic β Cells to Correct Diabetes in Allogeneic Mice. Gene Therapy, 16: 340-348, 2009.
R Gelling, P Vuguin, Xiu Du, L Cui, J Romer, R Pederson, M Leiser, H Sørensen, J Holst, C Fledelius, PB. Johansen, N Fleischer, C McIntosh, E Nishimura, and M Charron. Pancreatic β-cell overexpression of the glucagon recptor gene results in enhanced β-Cell function and mass. Am J Physiol Endocrinol Metab 2009, 297:E695-707 (PMID 19602585).
S Milman, K Witney, N.Fleischer. Metastatic medullary thyroid cancer presenting with elevatedlevels of CA 19-9 and CA 125. Thyroid 2011, 21:913-916.
Kuliawat R, Klein L, Gong Z, Nicoletta-Gentile M, Nemkal A, Cui L, Bastie C, Su K, Huffman D, Surana M, Barzilai N, Fleischer N and Muzumdar R. Potent Humanin Analog Increases Glucose-stimulated Insulin Secretion through Enhanced Metabolism in the Beta Cell. FASEBJ, 2013;27(12):4890-8.Epubb 2013 Aug 30, 2013. PMID:23995290
Milman S, Arnold J, Price M, Negassa A, Surks ML, FleischerN, Whitney KD. Medullary Thyroid Cancer that Stains Negative for CA19-9 has Decreased Metastatic Potential. Endocr Pract 2015 Feb 25:1-15 [Epub ahead of print] PMID: 2571629
Material in this section is provided by individual faculty members who are solely responsible for its accuracy and content.