Glutamine confers renoprotection by normalizing lipid and glutathione content in insulin-resistant pregnant rats.

Abstract

OBJECTIVE\nIncreasing consumption of fructose is a major contributor to epidemic metabolic syndrome (MS), and the risk of renal disorders and/or injuries remains high among individuals with MS particularly during pregnancy. Glutamine (GLT) has been demonstrated to have a modulatory effect in MS and/or insulin resistance (IR). This study investigated the effect of GLT on renal lipid accumulation and glutathione depletion induced by high fructose-enriched drink (FED) in pregnant rats and also tested the hypothesis that the renoprotective role of GLT is by suppression of adenosine deaminase (ADA)/xanthine oxidase (XO)/uric acid (UA) pathway.\n\n\nMETHODS\nPregnant Wistar rats weighing between 160 and 180\xa0g were allotted into Control, GLT, FED and FED\xa0+\xa0GLT groups (6rats/group). The groups received distilled water (vehicle, p. o.), 1\u202fg/kg bw GLT (p.o.), 10% Fructose (w/v) and 10% Fructose (w/v) plus 1\u202fg/kg bw GLT (p.o.) respectively, daily for 19 days.\n\n\nRESULTS\nData showed that FED caused IR, increased body weight gain, blood glucose, plasma insulin, creatinine, urea, lipid accumulation, lipid peroxidation, lactate production, aspartate transaminase and alanine aminotransferase, depressed Glucose-6-phosphate dehydrogenase, sodium-potassium-ATPase activities and glutathione. These alterations were accompanied by increased activity of ADA/XO/UA pathway. However, the FED-induced renal injury and its correlates were normalized by GLT supplementation.\n\n\nCONCLUSION\nThe present results demonstrate that renal lipid accumulation and glutathione depletion-driven renal injury in pregnant rats is accompanied by increased activity of ADA/XO/UA pathway. The findings also suggest that GLT would confer protection against renal injury by protecting against lipid accumulation and glutathionedepletion, at least in part, through suppression of ADA/XO/UA pathway.