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Scott Summers

Professor and Chair of Nutrition and Integrative Physiology and
Adjunct Professor of Biochemistry

Summers Photo

B.S. Indiana University

Ph.D. Southern Illinois University

Research

References

scott.a.summers@health.utah.edu

Scott Summers' Lab Page

Scott Summers' PubMed Literature Search

 

Molecular Biology Program

Biological Chemistry Program

Diabetes, dyslipidemia, metabolic disease, sphingolipids, ceramide, insulin resistance and beta cell failure

Research

My entire professional career has been devoted to the study of diabetes, with my interest having been born shortly after my father’s diagnosis with the disease.  My laboratory has become particularly interested in the relationship between dyslipidemia and metabolic disease and much of our current work derives from the observation that sphingolipids (e.g. ceramide) contribute to insulin resistance and beta cell failure, which are important features of the disease. Our current research efforts seek to identify the (a) site of sphingolipid function, (b) their mechanism of action, and (c) the regulatory events controlling sphingolipid accumulation.  Moreover, (d) we seek to develop drugs targeting enzymes in the ceramide-synthesizing pathway, which hold enormous potential in a broad spectrum of metabolic disorders.

References

  1. Meikle PJ and Summers SA (2017) Sphingolipids and phospholipids in insulin resistance and related metabolic disorders. Nature Reviews in Endocrinology and Metabolism 13 (2), 79-91
  2. Chaurasia B, Kaddai VA, Lancaster GL, Henstridge DC, Srirah S, Galam DAL, Gopalan, V, BPrahkash KNB, Velan SS, Bulchand S, Tson TJ, Wang M, Siddique MM, Yuguang G, Sigmundsson K, Mellet NA, Weir JM, Meikle PJ, Shabeeer BMMY, Shabbir A, Shayman JA, Hirabahashi Y, Shio SATE, Sugii S, and Summers SA (2016) Adipocyte ceramides regulate subcutaneous adipose browning, inflammation and metabolism. Cell Metabolism 24 (6), 820-834
  3. Goodpaster B and Summers SA (2016) CrossTalk Proposal: Intramyocellular ceramides do cause insulin resistance. Journal of Physiology 594 (12), 316703170
  4. Park M, Kaddai V, Ching J, Fridianto KT, Sieli RJ, Sugii S, and Summers SA (2016) Role for Ceramides, but NOT Sphingomyelins, as antagonists of insulin signaling and mitochondrial metabolism in C2C12 myotubes. Journal of Biological Chemistry 291 (46), 23978-23988
  5. Chaurasia B and Summers SA (2015) Ceramides—Lipotoxic inducers of metabolic disorders. Trends in Endocrinology and Metabolism 26 (10), 538-5041
  6. Siddique M, Li Y, Chaurasia B, Kaddai V and Summers SA (2015) Dihydroceramides – From bit players to lead actors. Journal of Biological Chemistry 290 (25), 15371-9
  7. Raichur S, Wang ST, Chan PW, Li Y, Ching J, Chaurasia B, Dogra S, Öhman M, Takeda K, Sugii S, Pewzner-Jung Y, Futerman AH, and Summers SA (2014) Increases in C16:0 Ceramides Resulting From CerS2 Haploinsufficiency Inhibits b-Oxidation and Confers Susceptibility to Diet-Induced Steatohepatitis and Insulin Resistance. Cell Metabolism 20 (4), 687-9542
  8. Holland WL, Bikman BT, Wang L-P, Sargent KM, Knotts TA, Shui G, Wenk MR, Pagliassotti MJ and Summers SA (2011) Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid-induced ceramide biosynthesis in mice. Journal of Clinical Investigation 121 (5), 1858-70
  9. Holland WL, Miller R, Wang ZV, Barth B, Bui HH, Halberg N, Davis KE, Wade M, Kuo M-S, Brozinick JT, Zhang BB, Birnbaum MJ, Summers SA and Scherer PE (2011) A unifying mechanism for adiponectin Action: the pleiotropic actions of adiponectin are mediated via receptor-mediated activation of neutral ceramidase activity. Nature Medicine 17 (1), 55-63
  10. Bikman BT and Summers SA (2011) Ceramides as modulators of cellular and whole-body metabolism. Journal of Clinical Investigation 11, 4222-4230
  11. Holland WL, Brozinick JT, Wang LP, Hawkins ED, Sargent KM, Liu Y, Narra K, Hoehn KL, Knotts TA, Siesky A, Nelson DH, Karathanasis SK, Fontenot GK, Birnbaum MJ and Summers SA (2007) Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistance. Cell Metabolism 5 (3), 167-79
Last Updated: 8/10/17