Laura Gabriela Sánchez‐Lozada

ORCID: 0000-0003-0348-9617
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About
Contact & Profiles
Research Areas
  • Diet, Metabolism, and Disease
  • Liver Disease Diagnosis and Treatment
  • Gout, Hyperuricemia, Uric Acid
  • Alcohol Consumption and Health Effects
  • Diet and metabolism studies
  • Thermoregulation and physiological responses
  • Chronic Kidney Disease and Diabetes
  • Case Reports on Hematomas
  • Electrolyte and hormonal disorders
  • Dialysis and Renal Disease Management
  • Birth, Development, and Health
  • Hormonal Regulation and Hypertension
  • Climate Change and Health Impacts
  • Garlic and Onion Studies
  • Nitric Oxide and Endothelin Effects
  • Genomics, phytochemicals, and oxidative stress
  • Metabolism and Genetic Disorders
  • Ion Transport and Channel Regulation
  • Acute Kidney Injury Research
  • Biochemical Acid Research Studies
  • Metabolism, Diabetes, and Cancer
  • Sodium Intake and Health
  • Curcumin's Biomedical Applications
  • Pharmacological Effects of Natural Compounds
  • Inflammasome and immune disorders

Instituto Nacional de Cardiología
2016-2025

Instituto Nacional de Cardiologia
1999-2021

University of Colorado Denver
2009-2021

National Institutes of Health
2015

University of Florida
2004-2013

Tecnológico Nacional de México
2013

Pediatric Nephrology of Alabama
2011-2013

University of Alabama
2011-2013

Istanbul Medeniyet University
2013

University of Colorado Anschutz Medical Campus
2010-2013

Increased consumption of fructose may play an important role in the epidemic metabolic syndrome and presage development diabetes, cardiovascular disease, chronic kidney disease. Once cell, is phosphorylated by ketohexokinase (KHK), leading to ATP, formation AMP, generation uric acid through xanthine oxidoreductase (XOR). This study aimed examine direct effects human proximal tubular cells (HK-2) whether they are mediated metabolism via KHK. At a similar concentration that observed peripheral...

10.1159/000381239 article EN cc-by-nc Annals of Nutrition and Metabolism 2015-01-01

Serum uric acid is commonly elevated in subjects with chronic kidney disease (CKD), but was historically viewed as an issue of limited interest. Recently, has been resurrected a potential contributory risk factor the development and progression CKD. Most studies documented that serum level independently predicts Raising rats can induce glomerular hypertension renal noted by arteriolosclerosis, injury tubulointerstitial fibrosis. Pilot suggest lowering plasma concentrations may slow While...

10.1093/ndt/gft029 article EN Nephrology Dialysis Transplantation 2013-03-29

Oxidative stress is known to be a major mechanism of endothelial dysfunction, which plays key role in the development cardiovascular disease. Although uric acid one most important antioxidants, recent studies have suggested that may causal dysfunction. In order understand paradoxical association with oxidative and vascular disease, we investigated whether induced human cells. We also examined acid-induced changes redox status were related aging death cells or an activation local...

10.1097/hjh.0b013e328337da1d article EN Journal of Hypertension 2010-03-23

Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, epidemiologically with renal progression. The hemodynamic effects fructose are unknown, as well different routes administration. Metabolic was induced rats over 8 wk by either a high-fructose diet (60%, F60, n = 7) or adding drinking water (10%, F10, 7). Body weight and food fluid each rat were measured weekly during follow-up. At baseline at end 8, systolic blood pressure, plasma uric acid,...

10.1152/ajprenal.00124.2006 article EN AJP Renal Physiology 2006-08-30

Endothelial dysfunction is a characteristic feature during the renal damage induced by mild hyperuricemia. The mechanism which uric acid reduces bioavailability of intrarenal nitric oxide not known. We tested hypothesis that oxidative stress might contribute to endothelial and glomerular hemodynamic changes occur with Hyperuricemia was in Sprague-Dawley rats administration uricase inhibitor, oxonic (750 mg/kg per day). superoxide scavenger, tempol (15 day), or placebo administered...

10.1152/ajprenal.00104.2008 article EN AJP Renal Physiology 2008-10-01

Fructose intake from added sugars has been implicated as a cause of nonalcoholic fatty liver disease. Here we tested the hypothesis that fructose may interact with high-fat diet to induce liver, and determine if this was dependent on key enzyme in metabolism, fructokinase. Wild-type or fructokinase knockout mice were fed low-fat (11%), (36%), (36%) high-sucrose (30%) for 15 weeks. Both wild-type developed obesity mild hepatic steatosis no evidence inflammation compared diet. In contrast,...

10.1002/hep.26594 article EN Hepatology 2013-06-28

<b><i>Background/Aims:</i></b> Endothelial dysfunction is associated with mitochondrial alterations. We hypothesized that uric acid (UA), which can induce endothelial in vitro and vivo, might also alter function. <b><i>Methods:</i></b> Human aortic cells were exposed to soluble UA measurements of oxidative stress, nitric oxide, density, ATP production, aconitase-2 enoyl Co-A hydratase-1 expressions, activity isolated mitochondria determined....

10.1159/000345509 article EN Nephron Experimental Nephrology 2012-12-07

Fructose intake from added sugars correlates with the epidemic rise in obesity, metabolic syndrome, and nonalcoholic fatty liver disease. also causes features of syndrome laboratory animals humans. The first enzyme fructose metabolism is fructokinase, which exists as two isoforms, A C. Here we show that fructose-induced prevented mice lacking both isoforms but exacerbated fructokinase A. Fructokinase C expressed primarily liver, intestine, kidney has high affinity for fructose, resulting...

10.1073/pnas.1119908109 article EN Proceedings of the National Academy of Sciences 2012-02-27

Excessive dietary fructose intake may have an important role in the current epidemics of fatty liver, obesity and diabetes as its parallels development these syndromes because it can induce features metabolic syndrome. The effects to hypertriglyceridemia insulin resistance, however, vary dramatically among individuals. first step metabolism is mediated by fructokinase (KHK), which phosphorylates fructose-1-phosphate; intracellular uric acid also generated a consequence transient ATP...

10.1371/journal.pone.0047948 article EN cc-by PLoS ONE 2012-10-24

The epidemic of chronic kidney disease in Nicaragua (Mesoamerican nephropathy) has been linked with recurrent dehydration. Here we tested whether dehydration may cause renal injury by activation the polyol pathway, resulting generation endogenous fructose that might subsequently induce via metabolism fructokinase. Wild-type and fructokinase-deficient mice were subjected to heat-induced One group each genotype was provided water throughout day other hydrated at night, after Both groups...

10.1038/ki.2013.492 article EN cc-by-nc-nd Kidney International 2013-12-11
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