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1656 E. Mabel Street
Primary Phone: (520) 6263709
1656 E. Mabel Street
Primary Phone: (520) 6263709
PhD, University of Arizona, 1986
MD, University of Arizona, 1997
- College Of Medicine
diabetes, hypertension, metabolic syndrome, insulin resistance resulting from physical inactivity, obesity and the metabolic syndrome; renin-angiotensin system (RAS), reactive oxygen species (ROS), and inflammation in skeletal muscle insulin signaling; insulin resistance and RAS on mitochondrial energy (ATP) production; identifying biological markers to predict progression of diabetes
Environmental Health Research & Expertise:
My laboratory investigates mechanisms contributing to insulin resistance that occur as a result of physical inactivity, obesity, and the cardiometabolic syndrome. We are particularly interested in defining the contribution of the renin-angiotensin-aldosterone system (RAAS), reactive oxygen species (ROS) and inflammation in preventing normal skeletal muscle insulin signaling. Skeletal muscle cell and tissue cultures, and whole animal responses to insulin by euglycemic-hyperinsulinemic clamp are used to study cellular insulin signaling pathways and tissue responses to insulin. I am also studying the effects of insulin resistance on mitochondrial energy (ATP) production in skeletal muscle and exercise capacity.
- MK-8825: a potent and selective CGRP receptor antagonist with good oral activity in rats.
- Erlotinib Associated Exacerbation of Hypothyroidism with Pericardial Tamponade.
- Adjusting for Urinary Creatinine Overestimates Arsenic Concentrations in Diabetics.
- Physical Activity in the Prevention of Chronic Kidney Disease.
- Nine days of intensive exercise training improves mitochondrial function but not insulin action in adult offspring of mothers with type 2 diabetes.
- Effect of glucose or fat challenge on aspirin resistance in diabetes.
- Clinical determinants of aspirin resistance in diabetes.
- Identification of potent, highly constrained CGRP receptor antagonists.
- Novel CGRP receptor antagonists through a design strategy of target simplification with addition of molecular flexibility.
- The discovery of highly potent CGRP receptor antagonists.
- Effect of renin inhibition and AT1R blockade on myocardial remodeling in the transgenic Ren2 rat.
- Skeletal muscle insulin resistance: role of inflammatory cytokines and reactive oxygen species.
- Angiotensin II-induced skeletal muscle insulin resistance mediated by NF-kappaB activation via NADPH oxidase.
- Caprolactams as potent CGRP receptor antagonists for the treatment of migraine.
- NADPH oxidase contributes to vascular inflammation, insulin resistance, and remodeling in the transgenic (mRen2) rat.
- Mineralocorticoid receptor blockade attenuates chronic overexpression of the renin-angiotensin-aldosterone system stimulation of reduced nicotinamide adenine dinucleotide phosphate oxidase and cardiac remodeling.
- Exercise and diet induced weight loss improves measures of oxidative stress and insulin sensitivity in adults with characteristics of the metabolic syndrome.
- Angiotensin II-mediated oxidative stress promotes myocardial tissue remodeling in the transgenic (mRen2) 27 Ren2 rat.
- Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor, decreases cardiac oxidative stress and remodeling in Ren2 transgenic rats.
- Albumin activation of NAD(P)H oxidase activity is mediated via Rac1 in proximal tubule cells.
- Inactivity induces increases in abdominal fat.
- Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat.
- Identification of novel, orally bioavailable spirohydantoin CGRP receptor antagonists.
- Angiotensin II-induced NADPH oxidase activation impairs insulin signaling in skeletal muscle cells.
- Benzodiazepine calcitonin gene-related peptide (CGRP) receptor antagonists: optimization of the 4-substituted piperidine.
- Oxidative stress and glomerular filtration barrier injury: role of the renin-angiotensin system in the Ren2 transgenic rat.
- Non-peptide calcitonin gene-related peptide receptor antagonists from a benzodiazepinone lead.
- Abrogation of oxidative stress improves insulin sensitivity in the Ren-2 rat model of tissue angiotensin II overexpression.
- Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts. Previous years
- Hypertension--a treatable component of the cardiometabolic syndrome: challenges for the primary care physician.
- The cardiometabolic syndrome as a cardiovascular risk factor.
- Oxidative stress in insulin-resistant conditions: cardiovascular implications.
- Impaired mitochondrial activity and insulin-resistant offspring of patients with type 2 diabetes.
- Insights into the biology of diabetic vascular disease: what's new?
- Exercise training prevents development of cardiac contractile dysfunction in hypertensive TG (mREN-2)27 rats.
- The key role of insulin resistance in the cardiometabolic syndrome.
- Effect of antihypertensive agents on the development of type 2 diabetes mellitus.
- Metabolic derangements in the insulin-resistant heart.
- Introduction: organ involvement in the cardiometabolic syndrome.
- Skeletal muscle insulin resistance is fundamental to the cardiometabolic syndrome.
- Obesity: are we prepared to act?
- Potent inhibitors of farnesyltransferase and geranylgeranyltransferase-I.
- Adrenal steroids and the metabolic syndrome.
- Methods in the evaluation of cardiovascular renin angiotensin aldosterone activation and oxidative stress.
- Skeletal muscle mitochondrial functions, mitochondrial DNA copy numbers, and gene transcript profiles in type 2 diabetic and nondiabetic subjects at equal levels of low or high insulin and euglycemia.
- The metabolic syndrome: role of skeletal muscle metabolism.