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.
Splice-specific Glycine Receptor Binding, Folding, and Phosphorylation of the Scaffolding Protein Gephyrin
