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Faculty Detail    
Name SUSHANT BHATNAGAR
  
Campus Address SHEL 1203 Zip 0012
Phone  205-996-0164
E-mail  sushantb@uab.edu
Other websites
     

Education
Graduate  West Virginia University, West Virginia     2008  Ph.D. 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med - Endocrinology, Diabetes & Metabolism Assistant Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Assistant Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Assistant Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cell, Molecular, & Developmental Biology 
Medical Scientist Training Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Post-graduate Training Post Doctoral Fellow, 2009–12, Department of Biochemistry, University of Wisconsin, Madison, WI Project: Positional cloning and initial functional characterization of tomosyn-2 gene underlying diabetes susceptible quantitative trait locus in an F2 mouse cross between obese diabetes resistant, C57BL/6 and diabetes susceptible, BTBR mice. Assistant Scientist, 2012–15, Department of Biochemistry, University of Wisconsin, Madison, WI Project 1: Identification of the mechanism by which beta cells regulate insulin secretion by modulating phosphorylation and ubiquitination-dependent degradation of tomosyn-2. Identification of an E3-ubiquitin ligase that regulates the abundance of tomosyn-2 protein. Project 2: Developed a high through-put bioinformatic method to identify novel proteins that are involved in regulating metabolic processes as a function of obesity, age, and diabetes. Honors And Awards 1. Oral presentation award (3rd place), Midwest Islet Club conference, Mentor (with Trung Huynh), 2017 2. UAB Honors College Experimental Fellowship Program, Mentor (with Trung Huynh), 2017 3. Young Investigator Travel Grant Award to the American Diabetes Association, San Diego, CA, 2017 4. Certificate of participation for receiving a top scoring abstract at the ADA Scientific Sessions, San Diego, CA, 2017 5. Keystone Scholarship, Pathogenesis of Diabetes, Santa Fe, NM; Jan 29–Feb 3, 2012 6. Best Poster Award, FASEB Summer Conferences: Molecular Mechanisms Involved in the Nutrient Control of Cellular Function, Carefree, Arizona; July, 20–25, 2008 7. Best Poster Award, E. J. Van Liere Convocation and Research Day, WVU, WV, 2008 8. Top 10 Abstracts for Oral Presentation, E. J. Van Liere Convocation and Research Day, West Virginia University, 2008 9. Pfizer Global Research and Development Scholarship Award: Keystone Symposia on Diabetes Mellitus, Insulin Action, and Resistance, Breckenridge,CO, 2008 10. Graduate Student Travel Award, School of Medicine, West Virginia University Funding 1. UAB DRC Pilot and Feasibility award, 5P30DK079626-10, 2017 2. NIH NIDDK, 4 R00 DK95975-03, 2016 3. NIDDK K99 NIH Pathways to Independence Award Grant #1K99DK095975-01, 2014 4. American Diabetes Association Mentor-Based Fellowship 7-11-MN-03 07/01/11-06/30/12 Press 1. Work featured “ Diabetes gene identified: tomosyn-2 regulates insulin secretion” in several national and international media (Science Daily, USA; Press Association, UK; Times of India, India; etc.), October 2011 2. Work featured, “WVU research shows new class of hormones may reverse diabetes and obesity: Graduate student’s presentation wins international award” Pittsburgh Post-Gazette, October 2008. Service Ad Hoc reviewer for Diabetologia, PLoS One, and Lipids in Health and Disease journals

Society Memberships
Organization Name Position Held Org Link
UAB Diabetes Research Center (DRC)  Member    
Endocrinology Society     
ASBMB   Menber   
American Diabetes Association  Member   
UAB Center for Excercise and Medicine   Associate Scientist   
UAB Nutritional and Obesity Research Center (NORC)  Member   http://www.norc.uab.edu/people/sbhatnagar 
Lab Website    https://www.bhatnagarlab.com 
 



Research/Clinical Interest
Title
Identification and characterization of novel factors in insulin secretion in obesity and type 2 diabetes
Description
Type 2 diabetes is a serious public health problem in the United States that affects more than 29 million individuals. Obesity is the leading cause of type 2 diabetes. During obesity, individuals develop resistance to insulin, which leads to increase in blood glucose levels. It is critical to maintain normal blood glucose levels. Therefore, to compensate for elevated blood glucose levels, pancreatic beta cells increase secretion of insulin to maintain euglycemia. When beta cell function fails, predominately during obesity, insulin secretion decreases and this leads to type 2 diabetes. It is well established that greater than 80% of type 2 diabetic individuals are obese, however, not all obese individuals are diabetic. This suggests that the reduction of insulin secretion from pancreatic beta cells leads to type 2 diabetes in obese individuals. Therefore, identifying factors that cause reduction in insulin secretion will improve our understanding of mechanisms underlying progression to type 2 diabetes. We employ genetics, bioinformatics, and proteomics approaches to identify novel regulators of beta-cell function. Our lab is currently focused on the following projects: Project 1: The role of tomosyn in insulin secretion. I positionally cloned tomosyn-2 by using a forward genetics approach as a gene that increases susceptibility to type 2 diabetes. Tomosyn-2 is an inhibitor of insulin secretion. It works by limiting the formation of the SNARE-mediated fusion of insulin granules to the plasma membrane. However, the mechanism of tomosyn-2 action still remains relatively uncharacterized. We are utilizing biochemical, cell biological, and physiological approaches to investigate the mechanism of tomosyn-2 in beta-cells. Currently, we are using knockout mouse models to understand the role of tomosyn-2 and its closely related protein tomosyn-1 in beta cell function. Project 2: The role of complement 1q-like 3 (C1ql3) protein in beta-cell function. Using bioinformatics approaches, our laboratory has identified a novel signaling pathway in pancreatic beta cells. We showed that C1ql3, which is a secreted protein signals in an autocrine-dependent manner via its G-protein coupled receptor to inhibit insulin secretion from pancreatic beta cells. By using knockout mice, we are identifying the mechanism by which C1ql3 and its receptor inhibits beta cell function. Understanding the role of these proteins will provide insight to the mechanism by which insulin secretion is reduced in obesity that leads to type 2 diabetes.

Positions Available
Date Posted Position Title
10/31/2018  Postdoctoral Scholar  
A postdoctoral position is immediately available within the basic, translational, and preclinical research program of the Department of Medicine in the Division of Endocrinology, Diabetes, Metabolism to study islet biology with the focus on understanding the regulation of insulin granule fusion from pancreatic beta-cells. The successful candidate will utilize knockout mouse models, molecular, pharmacological, and imaging (confocal with TIRFM) approaches to decipher the signaling pathways that regulate the formation of the SNARE complex in physiology, pathophysiology, and pathology states. The scope of this project also allows for the use of knockout mouse models to understand regulated secretion from non-beta cells in the disease states. Background in energy metabolism/secretory processes/islet biology is highly desirable. Prior experience in animal handling, cell culture, cloning, protein- and molecular-based assays is essential. Candidates with a Ph.D. in cell/molecular biology/physiology/pharmacology or a related discipline are encouraged to apply. Enthusiastic and highly-motivated candidates should submit a CV, a cover letter detailing research experience, and contact information of three references to Sushant Bhatnagar (Email: Sushantbhatnagar@uabmc.edu). Web links (https://www.bhatnagarlab.com and https://www.uab.edu/medicine/endocrinology/faculty).

About the University:
UAB pursues the frontiers of education, research and health care and strives to be one of the most dynamic and productive universities of the 21st century. Our strategic plan, Forging the Future, is our roadmap for the next five years of growth. It outlines goals that share three themes: increasing access to our world-class educational programs, patient care, and research; enhancing the alignment of people and programs to reflect the interdisciplinary nature of 21st-century curricula, scientific investigation, and creative scholarship; and investing in grand ideas to tackle major problems facing society.

The University of Alabama at Birmingham is an Equal Opportunity/Affirmative Action Employer committed to fostering a diverse, equitable and family-friendly environment in which all faculty and staff can excel and achieve work/life balance irrespective of, race, national origin, age, genetic or family medical history, gender, faith, gender identity and expression as well as sexual orientation. UAB also encourages applications from individuals with disabilities and veterans.

For more information on Equal Opportunity and Affirmative Action at UAB, visit the UAB Office of Diversity, Equity and Inclusion or call (205) 934-8762. Or contact the office at 701 20th Street South, AB 336, Birmingham, AL 35294-0103.
About our Postdoc office:
UAB is committed to the development and success of outstanding postdoctoral scientists. Here at UAB, nearly 300 postdoctoral fellows are training currently in a variety of disciplines, including dentistry, engineering, health professions, medicine, natural sciences and mathematics, public health, optometry, and social and behavioral sciences. Competitive postdoc awards are available including internships, grant incentives, funds to enhance education and collaboration outside UAB, and teaching opportunities at local universities. There is also a Postdoc Research Day with monetary awards. The OPE strongly encourages UAB research mentors to follow the National Research Service Award stipend level guidelines, and postdoctoral scholars qualify for health, life, and other insurances. They may also have the right to participate in the university’s 403(b) program and enjoy vacation, sick leave, maternity/paternity leave, and other benefits.
   
 

Selected Publications 
Publication PUBMEDID
Ren, G., Kim, T., Kim, H.S., Muccio, D., Atigadda, V.R., Grubbs, C.J., Itoh, N., Habegger, K.M., Young, M.E., Bhatnagar, S., Coric, T., Bjornsti, M.A., Shalev, A., Frank, S.J., and Kim, J-a (2018). A small molecule stimulating thermogenesis reverses diet-induced obesity. In preparation   
Hae-Suk Kim1, Ren, G., Kim, T., Bhatnagar, S., Yang, Q., Bahk, Y.Y., and Kim, Jeong-a (2018). Metformin reduces saturated fatty acid-induced lipid accumulation and inflammatory response by restoration of autophagic flux in endothelial cells. Under Revision FASEB   
Bethea, M., Liu, Y., Wade, A. K., Mullen, R., Gupta, R., Gelfanov, V., DiMarchi, R., Bhatnagar, S., Behringer, R., Habegger, K.M., Hunter, C (2018). Lhx1 is required for β-cell function via regulation of Glp1 receptor expression.Am J Physiol Endocrinol Metab. 2019 Mar 1;316(3): E397-E409  30620636 
Koltes, J.E., Gupta, R., Schiad, M., Appakalai, B., Kim, J-a., Kimple, M.E., and Bhatnagar, S (2018). A gene expression network analysis of the pancreatic islets from lean and obese mice identifies complement 1q-like-3 secreted protein as a regulator of beta-cell function. Under review, Scientific Reports    
Gupta, R., Koltes, J.E., Schiad, M., Appakalai, B., Kim, J-a., Kimple, M.E., and Bhatnagar, S (2018). The C1ql3 secreted protein inhibits insulin secretion by cell adhesion G-protein coupled receptor, BAI3 from pancreatic beta-cells. In press Journal of Biological Chemistry.   30228187 
ASF1B Chaperones Histone 3.3 to the beta-cell cycle dance.
Banerjee RR, Bhatnagar S.
Cell Cycle. 2016 Nov 18:0. 		 27860543 
Phosphorylation and degradation of tomosyn-2 de-represses insulin secretion.
Bhatnagar S, Soni MS, Wrighton LS, Hebert AS, Zhou AS, Paul PK, Gregg T, Rabaglia ME, Keller MP, Coon JJ, Attie AD.
J Biol Chem. 2014 Sep 5;289(36):25276-86. doi: 10.1074/jbc.M114.575985. Epub 2014 Jul 7. 		 25002582  
Downregulation of carnitine acyl-carnitine translocase by miRNAs 132 and 212 amplifies glucose-stimulated insulin secretion.
Soni MS, Rabaglia ME, Bhatnagar S, Shang J, Ilkayeva O, Mynatt R, Zhou YP, Schadt EE, Thornberry NA, Muoio DM, Keller MP, Attie AD.
Diabetes. 2014 Nov;63(11):3805-14. doi: 10.2337/db13-1677. Epub 2014 Jun 26. 		 24969106  
Positional cloning of a type 2 diabetes quantitative trait locus; tomosyn-2, a negative regulator of insulin secretion.
Bhatnagar S, Oler AT, Rabaglia ME, Stapleton DS, Schueler KL, Truchan NA, Worzella SL, Stoehr JP, Clee SM, Yandell BS, Keller MP, Thurmond DC, Attie AD.
PLoS Genet. 2011 Oct;7(10):e1002323. doi: 10.1371/journal.pgen.1002323. Epub 2011 Oct 6. 		 21998599  
Fibroblast growth factor-19, a novel factor that inhibits hepatic fatty acid synthesis.
Bhatnagar S, Damron HA, Hillgartner FB.
J Biol Chem. 2009 Apr 10;284(15):10023-33. doi: 10.1074/jbc.M808818200. Epub 2009 Feb 20. 		 19233843 
Chenodeoxycholic acid suppresses the activation of acetyl-coenzyme A carboxylase-alpha gene transcription by the liver X receptor agonist T0-901317.
Talukdar S, Bhatnagar S, Dridi S, Hillgartner FB.
J Lipid Res. 2007 Dec;48(12):2647-63. Epub 2007 Sep 6. 		 17823458  
 

Keywords
Energy Metabolism, Metabolic Disorders, Obesity, Type 2 Diabetes, Beta Cell Biology, Insulin Secretion, SNARE Biology, Secreted Proteins, Insulin Granule Trafficking, Tomosyn Proteins, Post-translational Modifications