A5002220484- Diet, Metabolism, and Disease
- Liver Disease Diagnosis and Treatment
- Diet and metabolism studies
- Cholesterol and Lipid Metabolism
- Cancer, Lipids, and Metabolism
- Alcohol Consumption and Health Effects
- Drug Transport and Resistance Mechanisms
- Renal Diseases and Glomerulopathies
- Renin-Angiotensin System Studies
- Sodium Intake and Health
- Sphingolipid Metabolism and Signaling
- Nitric Oxide and Endothelin Effects
University of California, Davis
2020-2022
Case Western Reserve University
2017-2020
The University of Melbourne
1997
Dietary fructose causes salt-sensitive hypertension. Proximal tubules (PTs) reabsorb 70% of the filtered NaCl. Angiotensin II (Ang II), atrial natriuretic peptide (ANP) and norepinephrine (NE) regulate this process. Although Ang signaling blockade ameliorates fructose-induced hypertension, basal PT Na+ reabsorption its sensitivity to aforementioned factors have not been studied in model. We hypothesized consuming with a high-salt diet selectively enhances transport II. investigated effects...
Fructose-enriched diets cause salt-sensitive hypertension. Proximal tubules (PTs) reabsorb 70% of the water and salt filtered through glomerulus. Angiotensin II (Ang II) regulates this process. Normally, dietary reduces Ang allowing kidney to excrete more salt, thereby preventing We hypothesized that fructose-enriched enhance ability low concentrations stimulate PT transport. measured effects a concentration (10-12 mol/L) on transport-related oxygen consumption (QO₂), Na/K-ATPase...
Angiotensin II exacerbates oxidative stress in part by increasing superoxide (O2-) production many renal tissues. However, whether it does so proximal tubules and the source of O2- this segment are unknown. Dietary fructose enhances stimulatory effect angiotensin on tubule Na+ reabsorption, but is true for We hypothesized that causes nephron stimulating NADPH oxidase (NOX)4-dependent decreasing amount antioxidant glutathione, exacerbated dietary fructose. measured basal II-stimulated with...
Angiotensin II (ANG II) stimulates proximal nephron transport via activation of classical protein kinase C (PKC) isoforms. Acute fructose treatment PKC and dietary enhances ANG II’s ability to stimulate Na + transport, but the mechanisms are unclear. We hypothesized that renal tubule reabsorption by augmenting PKC-α increases in intracellular Ca 2+ . measured total isoform-specific activity, basal II-stimulated oxygen consumption, a surrogate reabsorption, tubules from rats given either 20%...
Metastatic castration-resistant prostate cancer (mCRPC) features high intratumoral cholesterol levels, due to aberrant regulation of homeostasis. However, the underlying mechanisms are still poorly understood. The retinoid acid receptor-related orphan receptor gamma (RORγ), an attractive therapeutic target for and autoimmune diseases, is strongly implicated in progression. We demonstrate this study that mCRPC cells tumors, RORγ plays a crucial role deregulation First, we found activates...
Dietary fructose consumption has increased dramatically over the past four decades in part due to of sugary beverages. Rats ingesting a diet that includes 20 % drinking water develop salt‐sensitive hypertension. This is an sensitivity proximal nephron angiotensin II (Ang II), which stimulates Na reabsorption this segment at physiological concentrations via increases reactive oxygen species such as superoxide (O2−). Thus we hypothesized dietary enhances ability Ang stimulate O2− production by...
Dietary fructose causes salt-sensitive hypertension. This is in part due to increasing the sensitivity of proximal nephron Na reabsorption angiotensin II (Ang II) such that lower concentrations stimulate transport a greater extent. Ang stimulates this segment by protein kinase C (PKC) α, calcium- and lipid-dependent kinase. We hypothesized dietary increases ability elevate intracellular calcium (Cai) and, thereby, activate PKC α tubules. This, turn, Na/H exchange activity, primary...