Effect of glycine on the cyclooxygenase pathway of the kidney arachidonic acid metabolism in a rat model of metabolic syndrome
Autor: | Eulises Díaz-Díaz, Israel Pérez-Torres, Pedro Flores, Natalia Pavón, Oscar Infante, Blanca Ibarra, Elizabeth Soria-Castro, Guadalupe Baños, Rocío Torrico-Lavayen |
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Rok vydání: | 2011 |
Předmět: |
Male
medicine.medical_specialty Physiology medicine.medical_treatment Anti-Inflammatory Agents Glycine Prostaglandin Renal function Blood Pressure Kidney Cyclooxygenase pathway chemistry.chemical_compound Physiology (medical) Internal medicine Diabetes mellitus medicine Animals Rats Wistar Metabolic Syndrome Pharmacology Arachidonic Acid biology Insulin Body Weight General Medicine medicine.disease Disease Models Animal Endocrinology medicine.anatomical_structure chemistry Prostaglandin-Endoperoxide Synthases biology.protein Arachidonic acid Cyclooxygenase Signal Transduction |
Zdroj: | Canadian Journal of Physiology and Pharmacology. 89:899-910 |
ISSN: | 1205-7541 0008-4212 |
Popis: | The kidneys are organs that can be severely impaired by metabolic syndrome (MS). This is characterized by the association of various pathologies such as hypertension, dyslipidemia, and type-2 diabetes. Glycine, a nonessential amino acid, is known to possess various protective effects in the kidney, such as a decrease in the deterioration of renal function and a reduction of the damage caused by hypoxia. In a rat model of MS, the effect of glycine on the cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism was studied in isolated perfused kidney. MS was induced in Wistar rats by feeding them a 30% sucrose solution for 16 weeks. The addition of 1% glycine to their drinking water containing 30% sucrose, for 8 weeks, reduced high blood pressure, triglyceride levels, insulin concentration, homeostatis model assessment (HOMA) index, albuminuria, AA concentration in kidney homogenate, renal perfusion pressure, prostaglandin levels, PLA2expression, and COX isoform expression, compared with MS rats that did not receive the glycine supplement. Glycine receptor expression decreased significantly with MS, but glycine treatment increased it. The results suggest that in the MS model, 1% glycine treatment protects the kidney from damage provoked by the high sucrose consumption, by acting as an anti-inflammatory on the COX pathway of AA metabolism in kidney. |
Databáze: | OpenAIRE |
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