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. Yang K (11/05/2019). Soluble (Pro)renin receptor as a potential therapy for diabetes insipidus.
  2. Pike D (02/2019). The effect of endothelial nitric oxide synthase on the hemodynamics and wall mechanics in murine arteriovenous fistulas. Sci Rep.
  3. C Petersen (01/2019). Dietary supplementation with strawberry induces marked changes in the composition and functional potential of the gut microbiome in diabetic mice.
  4. Park S-K (01/2019). Elevated arterial shear rate increases indices of endothelial cell autophagy and nitric oxide synthase activation in humans.
  5. Petersen C (07/15/2018). Circulating metabolites of strawberry mediate reductions in vascular inflammation and endothelial dysfunction in db/db mice.
  6. Bharat D (01/2018). Blueberry metabolites attenuate lipotoxicity-induced endothelial dysfunction.
  7. Dey P (11/2017). Improved hepatic y-tocopherol status limits oxidative and inflammatory stress-mediated liver injury in db/db mice with nonalcoholic steatohepatits.
  8. Yang K (11/2017). The soluble (pro)renin receptor does not influence lithium-induced diabetes insipidus but does provoke beiging of white adipose tissue in mice. . Physiol Rep.
  9. Hydren JR (10/15/2017). Are cardiovascular reflexes sensitive to subtle alterations in arterial waveform patterns? J Appl Physiol (1985).
  10. Bharat D (10/12/2017). Blueberry Metabolites Attenuate Lipotoxicity-Induced Endothelial Dysfunction.
  11. Qian Y (09/11/2017). Metabolites of flavonoid compounds preserve indices of endothelial cell nitric oxide bioavailability under glucotoxic conditions. .
  12. Qian Y (09/11/2017). Metabolites of flavonoid compounds preserve indices of enothelial cell nitric oxide bioavailability under glucotoxic conditions.
  13. Bharath LP (06/2017). Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent purinergic signaling to eNOS. Arterioscler Thromb Vasc Biol.
  14. Pires KM (01/2017). Autophagy inhibition in (ob/ob) hears is mediated by mTOR signaling that may be independent of Akt. . J Mol Cell Cardiol.
  15. Bharath LP (01/2017). Endothelial cell autophagy maintains shear stress-induced nitric oxide generation via glycolysis-dependent purinergic signaling to eNOS.
  16. Li Y (12/2016). y-Carboxyethyl hydroxychroman, a metabolite of γ−tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose. Exp Biol Med.
  17. Li Y (01/2016). y-Carboxyethyl hydroxychroman, a metabolite of γ−tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose. Exp Biol Med.
  18. Bharath LPRuan TLi YRavindran AWan XNhan JKWalker MLDeeter LGoodrich RJohnson EMunday D (11/01/2015). Ceramide-Initiated Protein Phosphatase 2A Activation Contributes to Arterial Dysfunction in Vivo.
  19. Park SYIves SGifford JAndtbacka RHyngstrom JReese VLayec GBharath LPSymons JDRichardson R (07/15/2015). The impact of age on the vasodilatory function of human skeletal muscle feed arteries. Am J Physiol Heart Circ Physiol.
  20. Kwon OSTanner REBarrows KMRuntsch MSymons JD Jalili TBikman BMcClain DOConnell RDrummond M (07/01/2015). MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling, and glucose intolerance. .
  21. Barbarroja N (04/2015). Increased dihydroceramide/ceramide ratio mediated by defective expression of degs1 impairs adipocyte differentiation and function. (Read full article)
  22. Bharath LP (07/2014). Impairment of autophagy in endothelial cells prevents shear-stress-induced increases in nitric oxide bioavailability. Can J Physiol Pharmacol.
  23. Bosse JD (06/2013). A low-carbohydrate/high-fat diet reduces blood pressure in spontaneously hypertensive rats without deleterious changes in insulin resistance.
  24. Symons JD (06/2013). Opportunity "Nox" : a novel approach to preventing endothelial dysfunction in the context of insulin resistance. .
  25. Symons JD (06/2013). Lipotoxicity contributes to endothelial dysfunction : a focus on the contribution from ceramide.
  26. Zhang QJ (06/2012). Ceramide mediates vascular dysfunction in diet-induced obesity by pp2a-mediated dephosphorylation of the enos-akt complex. .
  27. Miller CJ (06/2012). Disruption of nrf2/are signaling impairs antioxidant mechanisms and promotes cell degradation pathways in aged skeletal muscle.
  28. Larson A (06/2012). Therapeutic potential of quercetin to decrease blood pressure: review of efficacy and mechanisms. . Adv Nutr.
  29. Wende AR (06/2012). Mechanisms of lipotoxicity in the cardiovascular system. Curr Hypertens Rep.
  30. Ives SJ (06/2011). Human skeletal muscle feed arteries studied in vitro: the effect of temperature on α(1)-adrenergic responsiveness. Exp Physiol.
  31. Larson AJ (07/2010). Quercetin: A treatment for hypertension?
  32. Tanner JM (06/2010). Fasting-induced reductions in cardiovascular and metabolic variables occur sooner in obese versus lean mice. Exp Biol Med.
  33. Gonzalez F J (01/2009). Distinct Functions of Vascular Endothelial and Smooth Muscle PPAR in Regulation of Blood Pressure and Vascular Tone. 37(1), 21-27. (Read full article)
  34. Mullick AE (01/2006). Hyperhomocysteinemia increases arterial permeability and stiffness in mice. .
  35. Pettitt RW (06/2005). Eccentric strain at long muscle length evokes the repeated bout effect.
  36. Rendig SV (11/01/2003). Effects of statins on myocardial and coronary artery response to ischemia-reperfusion. Can J Physiol Pharmacol.
  37. Longhurst JC (06/1993). Function and Development of Coronary Collateral Vessels. Collateral Circulation.

Other

  1. Singhal AK (07/2010). Role of endothelial cells in myocardial ischemia-reperfusion injury. . Vasc Dis Prev. Vascular Disease Prevention.