J. David Symons

J. David Symons, PhD

Academic Information

Departments Adjunct - Internal Medicine

Divisions: Endocrinology

1990-94 Assistant Research Physiologist Department of Internal Medicine, Division of Cardiovascular Medicine University of California, Davis; Davis, California

1994-95 Senior Research Scientist Department of Cardiovascular Pharmacology Alliance Pharmaceutical Corporation; San Diego, California

1995-2001 Assistant Adjunct Professor Department of Internal Medicine, Division of Cardiovascular Medicine University of California, Davis; Davis, California

2001-05 Assistant Professor University of Utah, College of Health, Department of Exercise Sport Science; Salt Lake City, Utah

2006-Present Professor University of Utah, College of Health, Department of Nutrition and Integrative Physiology; Salt Lake City, Utah

2007-Present Adjunct Associate Professor University of Utah, School of Medicine, Department of Internal Medicine, Division of Endocrinology, Metabolism, and Diabetes; Salt Lake City, Utah

2013-Present Professor, University of Utah, College of Health, Kinesiology

2014-Present Investigator, University of Utah Molecular Medicine Program

After my second postdoctoral fellowship at UC Davis, I was appointed to the faculty in the School of Medicine at UC Davis until I moved to the University of Utah in 2001. I have a primary appointment in the College of Health, Department of Nutrition and Integrative Physiology, Adjunct appointment in Endocrinology, Metabolism, and Diabetes (my lab is in the Eccles Institute of Human Genetics), I am an Investigator in the University of Utah Molecular Medicine Program, a member of Diabetes and Metabolism Center, and the Center on Aging.

Research Statement

Our laboratory investigates vascular function in response to pathophysiological (e.g., obesity/type 2 diabetes, ischemia, hypertension), physiological (e.g., aging, physical exercise), and nutritional (e.g., polyphenolic compounds, metabolites of polyphenolic compounds) interventions. To do so, we use immortalized cells, primary human and rodent cells, isolated blood vessels, intact animals, and humans.

Selected Publications

Journal Article

  1. Tanner J (2010). Fasting-induced reductions in cardiovascular and metabolic variables occur sooner in obese versus lean mice. Experimental biology and medicine,
  2. Zhang Q (2012). Ceramide mediates vascular dysfunction in diet-induced obesity by pp2a-mediated dephosphorylation of the enos-akt complex.
  3. Li (2016). y-Carboxyethyl hydroxychroman, a metabolite of ¿¿tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose. Experimental biology and medicine,
  4. Ives S (2011). Human skeletal muscle feed arteries studied in vitro: the effect of temperature on ¿(1)-adrenergic responsiveness. Experimental physiology,
  5. Miller C (2012). Disruption of nrf2/are signaling impairs antioxidant mechanisms and promotes cell degradation pathways in aged skeletal muscle.
  6. Pettitt R (2005). Eccentric strain at long muscle length evokes the repeated bout effect.
  7. Bharath L (2017). Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent purinergic signaling to eNOS. Arteriosclerosis, thrombosis, and vascular biology,
  8. Bharath L (2014). Impairment of autophagy in endothelial cells prevents shear-stress-induced increases in nitric oxide bioavailability. Canadian journal of physiology and pharmacology,
  9. Gonzalez, F. J (2009). Distinct Functions of Vascular Endothelial and Smooth Muscle PPAR in Regulation of Blood Pressure and Vascular Tone. 37(1), 21-27.
  10. Dey (2017). Improved hepatic y-tocopherol status limits oxidative and inflammatory stress-mediated liver injury in db/db mice with nonalcoholic steatohepatits.
  11. Yang (2019). Soluble (Pro)renin receptor as a potential therapy for diabetes insipidus.
  12. C Peterse (2019). Dietary supplementation with strawberry induces marked changes in the composition and functional potential of the gut microbiome in diabetic mice.
  13. Barbarroja, N (2015). Increased dihydroceramide/ceramide ratio mediated by defective expression of degs1 impairs adipocyte differentiation and function.
  14. Park SY,Ives S,Gifford J,Andtbacka R,Hyngstrom J,Reese V,Layec G,Bharath LP,Symons JD,Richardson (2015). The impact of age on the vasodilatory function of human skeletal muscle feed arteries. American journal of physiology. Heart and circulatory physiology,
  15. Mullick A (2006). Hyperhomocysteinemia increases arterial permeability and stiffness in mice.
  16. Longhurst J (1993). Function and Development of Coronary Collateral Vessels. Collateral Circulation.
  17. Pike (2019). The effect of endothelial nitric oxide synthase on the hemodynamics and wall mechanics in murine arteriovenous fistulas. Scientific reports,
  18. Bharath L (2017). Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent purinergic signaling to eNOS.
  19. Wende A (2012). Mechanisms of lipotoxicity in the cardiovascular system. Current hypertension reports,
  20. Pires K (2017). Autophagy inhibition in (ob/ob) hears is mediated by mTOR signaling that may be independent of Akt. Journal of molecular and cellular cardiology,
  21. Li (2016). y-Carboxyethyl hydroxychroman, a metabolite of ¿¿tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose. Experimental biology and medicine,
  22. Kwon OS,Tanner RE,Barrows KM,Runtsch M,Symons JD, Jalili T,Bikman B,McClain D,OConnell R,Drummond (2015). MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling, and glucose intolerance.
  23. Bharat (2018). Blueberry metabolites attenuate lipotoxicity-induced endothelial dysfunction.
  24. Bharat (2017). Blueberry Metabolites Attenuate Lipotoxicity-Induced Endothelial Dysfunction.
  25. Larson (2012). Therapeutic potential of quercetin to decrease blood pressure: review of efficacy and mechanisms. Advances in nutrition (Bethesda, Md.),
  26. Hydren J (2017). Are cardiovascular reflexes sensitive to subtle alterations in arterial waveform patterns?. Journal of applied physiology (Bethesda, Md.,
  27. Yang (2017). The soluble (pro)renin receptor does not influence lithium-induced diabetes insipidus but does provoke beiging of white adipose tissue in mice. Physiological reports,
  28. Larson A (2010). Quercetin: A treatment for hypertension?.
  29. Symons J (2013). Opportunity "Nox" : a novel approach to preventing endothelial dysfunction in the context of insulin resistance.
  30. Petersen (2018). Circulating metabolites of strawberry mediate reductions in vascular inflammation and endothelial dysfunction in db/db mice.
  31. Bosse JD (2013). A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance.
  32. Qian (2017). Metabolites of flavonoid compounds preserve indices of enothelial cell nitric oxide bioavailability under glucotoxic conditions.
  33. Qian (2017). Metabolites of flavonoid compounds preserve indices of endothelial cell nitric oxide bioavailability under glucotoxic conditions.
  34. Rendig S (2003). Effects of statins on myocardial and coronary artery response to ischemia-reperfusion. Canadian journal of physiology and pharmacology,
  35. Symons J (2013). Lipotoxicity contributes to endothelial dysfunction : a focus on the contribution from ceramide.
  36. Bharath LP,Ruan T,Li Y,Ravindran A,Wan X,Nhan JK,Walker ML,Deeter L,Goodrich R,Johnson E,Munday (2015). Ceramide-Initiated Protein Phosphatase 2A Activation Contributes to Arterial Dysfunction in Vivo.
  37. Park S- (2019). Elevated arterial shear rate increases indices of endothelial cell autophagy and nitric oxide synthase activation in humans.

Other

  1. Singhal A (2010). Role of endothelial cells in myocardial ischemia-reperfusion injury. Vascular disease prevention,