Sayeepriyadarshini Anakk

Sayeepriyadarshini Anakk
Sayeepriyadarshini Anakk
(217) 300-7905
453 Medical Sciences Building


  • Postdoctoral Fellow, 2006-2012, Baylor College of Medicine, Houston, Texas
  • Ph.D., 2000-2005, Biochemistry & Molecular Biology, GSBS, University of Texas Health Science Center- Houston

Academic Positions

  • 2013- Present: Assistant Professor at the University of Illinois, Urbana-Champaign
  • Affiliate, Division of Nutritional Sciences
  • Affiliate, Beckman Institute
  • Molecular Integrative Physiology

Research Interests

  • Obesity and diabetes have emerged as major epidemics and are now recognized as modern life style diseases. Several nuclear receptors have been implicated in regulating fat and glucose homeostasis. We are interested in characterizing the tissue specific roles for Farnesoid X Receptor (Fxr) and its principal target Small Heterodimer Partner (Shp) in regulating the energy metabolism. It is known that both Fxr-/- mice as well as Shp-/- mice are glucose intolerant. Consistent with these data, SNPs in Fxr are associated with fasting hyperglycemia and mutations in the Shp gene are associated with obesity. These findings highlight the importance of Fxr-Shp axis in controlling fat and glucose metabolism. We have recently discovered that combined loss of both Fxr and Shp, lead to an unexpected reduction in fat depots, enhanced glucose control, and resistance to diet induced obesity which is in stark contrast with the results from individual Fxr-/- mice as well as Shp-/- mice. Therefore we will investigate the coordinate role for both Fxr and Shp in protecting against obesity and subsequent diabetes. Apart from regulating fat and glucose Fxr and Shp play a crucial role in bile acid homeostasis. Bile acids are now recognized to affect wide range of cellular functions including fat and glucose metabolism, mitochondrial function, and the composition of the gut microbiota. My laboratory is interested in understanding (i) How bile acids confer resistance to diet-induced obesity? (ii) What are roles for Fxr and Shp in controlling fat metabolism? and (iii) How and When do bile acids cross-talk with the gut microbiota.

Other Publications

  • Desai MS*, Mathur B*, Eblimit Z, Vasquez H, Taegtmeyer H, Karpen SJ, Penny DJ, Moore DD, Anakk S. Bile acid excess induces cardiomyopathy and metabolic dysfunctions in the heart. Hepatology. 2017 Jan; 65(1)189-201. doi: 10.1002/hep.28890. Epub 2016 Nov 29. PMID: 27774647 * denotes equal authorship.
  • Kim KH, Choi S, Zhou Y, Kim EY, Lee JM, Saha PK, Anakk S, Moore DD. Hepatic FXR/SHP axis modulates systemic glucose and fatty acid homeostasis in aged mice. Hepatology. 2017 Aug;66(2):498-509. doi: 10.1002/hep.29199. Epub 2017 Jun 26. PMID: 28378930
  • Akinrotimi O*, Riessen R*, VanDuyne P, Park JE, Wong LJ, Zavacki AM, Schoonjans K, Anakk S (*Co-first author). Shp deletion prevents hepatic steatosis and when combined Fxr loss protects against type 2 diabetes. Hepatology. 2017 Jun 6. doi: 10.1002/hep.29305. [Epub ahead of print]. PMID: 28586124


  • David L Williams Award Runner up Kern Lipid Conference, Vail, Colorado (2017)
  • Oral Presentation and Travel Award, 19th International Symposium on the Cells of the Hepatic Sinusoid, Galway, Ireland (2017)
  • Outstanding Advisor Award, Medical Scholars Program, University of Illinois, Urbana-Champaign, IL (2016)
  • Presidential Poster Judge, Annual Endocrine Society meeting, Boston, MA (2016)
  • Travel Award, South East Lipid Research Conference, Atlanta, Georgia (2015)

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