Thunder Jalili

Thunder Jalili, PhD

Languages spoken: Western Farsi

Academic Information

Departments Primary - , Adjunct -

Academic Office Information

thunder.jalili@utah.edu

Thunder Jalili received his Ph.D. from The Ohio State University in Nutrition with specialization in Biochemistry & Molecular Biology. Following graduate school Dr. Jalili completed postdoctoral fellowships at The Harvard School of Public Health in the Department of Cancer Biology, and at the University of Cincinnati Medical Center in the Division of Cardiology. He joined the faculty at the University of Utah in 1999 and is currently an Associate Professor in the Department of Nutrition & Integrated Physiology and Director of Graduate Studies.

Research Statement

Cardiovascular disease (CVD) is the most prevalent public health problem facing the United States and the rest of the Western world. Many researchers believe that diet is critical for both prevention and treatment of CVD. To this end my research is focused on understanding how cardiovascular function and metabolism can be regulated by consumption of macronutrients, as well as supplementation with magnesium, and dietary phytochemicals. The goals of my research are to determine efficacy of supplements and diet therapy, and answer questions regarding optimum dosage and mechanisms of action.

Selected Publications

Journal Article

  1. Priyankar Dey P (01/01/2019). Improved hepatic γ-tocopherol status limits oxidative and inflammatory stress-mediated liver injury in db/db mice with nonalcoholic steatohepatitis. .
  2. Anandh Babu PV (01/01/2019). Dietary supplementation with strawberry induces marked changes in the composition and functional potential of the gut microbiome in diabetic mice.
  3. Bharat D (01/01/2018). Blueberry metabolites attenuate lipotoxicity-induced endothelial dysfunction. . 62(2).
  4. Qian Y (09/01/2017). Metabolites of flavonoid compounds preserve indices of endothelial cell nitric oxide bioavailability under glucotoxic conditions. Nutr Diabetes, 11:7(9).
  5. Li Y (12/01/2016). 5. Carboxyethyl Hydroxychroman, a metabolite of tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose. . 18, 2056-2062.
  6. Li Y Bharath LP Qian Y Ruan T Anandh Babu PV Bruno RS Symons JD Jalili T (07/01/2016). γ-Carboxyethyl hydroxychroman, a metabolite of γ-tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose.
  7. Chen X (03/2016).
  8. Biesinger S Michaels HA Quadros AS Qian Y Rabovsky AB Badger RS Jalili T (01/01/2016). A combination of isolated phytochemicals and botanical extracts lowers diastolic blood pressure in a randomized controlled trial of hypertensive subjects. Eur J Clin Nutr, 70, 10-6.
  9. Kwon Oh Sung (2015). MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling and glucose intolerance. ajpendo.00124.2015.
  10. Kwon OS (07/2015).
  11. Agergaard J (2014). Skeletal Muscle Ras-Related GTP Binding B mRNA and Protein Expression Is Increased after Essential Amino Acid Ingestion in Healthy Humans. 144(9), 1409-1414.
  12. Carlin MB (07/2014).
  13. Abel E D (2013). A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance. 304(12), H1733-H1742.
  14. Bruno Richard S (2013). Dietary fat increases quercetin bioavailability in overweight adults. 57(5), 896-905.
  15. Bosse JD (06/15/2013).
  16. Guo Yi (02/2013).
  17. Jalili Thunder (2012). Acute, quercetin-induced reductions in blood pressure in hypertensive individuals are not secondary to lower plasma angiotensin-converting enzyme activity or endothelin-1: nitric oxide. 32(8), 557-564.
  18. Nunthakungwan Orathai (2012). Cytosolic, but not mitochondrial, oxidative stress is a likely contributor to cardiac hypertrophy resulting from cardiac specific GLUT4 deletion in mice: Cardiac specific GLUT4 deletion and oxidative stress. 279(4), 599-611.
  19. Symons J D (2012). Therapeutic Potential of Quercetin to Decrease Blood Pressure: Review of Efficacy and Mechanisms. 3(1), 39-46.
  20. Larson AJ (08/2012).
  21. Jalili T (01/2012).
  22. Symons J David (2010). Quercetin: A Treatment for Hypertension?—A Review of Efficacy and Mechanisms. 3(1), 237-250.
  23. Guo Y (2009). Acute Quercetin Supplementation Does Not Lower Blood Pressure or Ace Activity in Normotensive Males. 109(9), A16.
  24. Hu E (2009). Mammalian Target of Rapamycin Is a Critical Regulator of Cardiac Hypertrophy in Spontaneously Hypertensive Rats. 54(6), 1321-1327.
  25. Soesanto WS (10/2009).
  26. Carlstrom J (07/2007).
  27. Edwards RL (07/2007).
  28. Jalili T (07/2006).
  29. Itoh S (2005). Role of p90 Ribosomal S6 Kinase (p90RSK) in Reactive Oxygen Species and Protein Kinase C (PKC- )-mediated Cardiac Troponin I Phosphorylation. 280(25), 24135-24142.
  30. Arvizo Joel (2005). 5(1), 6.
  31. Jalili T (09/2005).
  32. Itoh S (06/2005).
  33. Heap J (04/2004).
  34. Jalili T (02/2003).
  35. DiSilvestro RA (11/2000).
  36. Jalili T (09/1999).
  37. Takeishi Y (06/1999).
  38. Takeishi Y (05/1999).
  39. Jalili T (10/1998).
  40. Jalili T (02/1997).
  41. Jalili T (04/1996).

Review

  1. Larson AJ (02/2012). [Review].
  2. Larson AJ (07/2010). [Review].
  3. Jalili T (10/2000). [Review].
  4. Jalili T (03/1999). [Review].