Stress oxydant et effets bénéfiques rénaux de la restriction sodée dans l’insulinorésistance chez le rat

No abstract is available for this paper.

• Publication year

  2012

• Venue

  Annales De Cardiologie Et D Angeiologie

• Publication date

  2012-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.ANCARD.2012.04.017
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

• Endocrinological aspects of proteinuria and podocytopathy in diabetes: role of the aldosterone/mineralocorticoid receptor system.

  2011cited by this paper
• Dietary fructose causes tubulointerstitial injury in the normal rat kidney.

  2010influential reference
• Critical role of Nox4-based NADPH oxidase in glucose-induced oxidative stress in the kidney: implications in type 2 diabetic nephropathy.

  2010cited by this paper
• Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?

  2009cited by this paper
• Microalbuminuria—A Biomarker of Renal Microvascular Disease

  2009cited by this paper
• Inhibition of NADPH Oxidase Prevents Advanced Glycation End Product–Mediated Damage in Diabetic Nephropathy Through a Protein Kinase C-α–Dependent Pathway

  2008cited by this paper
• Validation of simple indexes to assess insulin sensitivity during pregnancy in Wistar and Sprague-Dawley rats.

  2008cited by this paper
• Effect of PPAR-gamma agonist on adiponectin levels in the metabolic syndrome: lessons from the high fructose fed rat model.

  2007cited by this paper
• Fructose, but not dextrose, accelerates the progression of chronic kidney disease.

  2007influential reference
• Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy.

  2006cited by this paper
• Cardiorenal abnormalities associated with high sodium intake: correction by spironolactone in rats.

  2005cited by this paper
• Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome

  2005cited by this paper
• Involvement of oxidative stress and NADPH oxidase activation in the development of cardiovascular complications in a model of insulin resistance, the fructose-fed rat.

  2005cited by this paper
• Dietary fish oil prevents vascular dysfunction and oxidative stress in hyperinsulinemic rats.

  2005cited by this paper
• Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension.

  2003cited by this paper
• The renin-angiotensin and adrenergic nervous system in cardiac hypertrophy in fructose-fed rats.

  2002cited by this paper
• Production of superoxide through NADH oxidase in thick ascending limb of Henle's loop in rat kidney.

  2002cited by this paper
• Long-term fructose intake: biochemical consequences and altered renal histology in the male rat.

  2002cited by this paper
• Dietary sodium and target organ damage in essential hypertension.

  2002cited by this paper
• Candesartan prevents L-NAME-induced cardio-renal injury in spontaneously hypertensive rats beyond hypotensive effects

  2001cited by this paper
• Production and Actions of Superoxide in the Renal Medulla

  2000cited by this paper
• Bosentan reduces blood pressure and the target-organ damage induced by a high-fructose diet in rats.

  1999cited by this paper
• High Fructose‐Fed Rats: A Model of Glomerulosclerosis Involving The Renin‐Angiotensin System and Renal Gelatinases

  1999cited by this paper
• Angiotensin II induces superoxide anion production by mesangial cells.

  1998cited by this paper
• Fructose-induced insulin resistance and hypertension in rats.

  1987cited by this paper

• Glucose Oxidase Induces Cellular Senescence in Immortal Renal Cells through ILK by Downregulating Klotho Gene Expression

  2015cites this paper
• [Sodium restriction prevents cardiovascular remodeling associated with insulin-resistance in the rat].

  2013cites this paper
• Sodium restriction on top of renin–angiotensin–aldosterone system blockade increases circulating levels of N-acetyl-seryl-aspartyl-lysyl-proline in chronic kidney disease patients

  2013cites this paper