L-Arginine’s Glucose Homeostatic Influence in Renal Damaged Wistar Rats is Possibly Mediated by Adiponectin Expression

Abstract

Hypoglycemia, as a direct result of the glucosuria is usually seen in patients with acute kidney injury hence glucose homeostasis is disturbed. The compensatory effect of adiponectin in the insulin deficient state is documented. We previously demonstrated that L-arginine enhances glucose transport mechanisms in renal-damaged rats. The current study was designed to investigate possible glucose handling synergy between L-arginine and adiponectin in Wistar rats induced with acute kidney injury. Twenty four rats weighing between 120g-150g were divided into 4 groups of six rats each. Group 1 (Control) had normal feed and water; Group 2 (Untreated) was induced with AKI and left untreated. Group 3 and 4 took 50mg/kg and 500mg/kg L-arginine respectively after AKI induction. Acute kidney injury was induced by intra-muscular injection of glycerol (50% solution, 8 ml/kg BW). Oral glucose tolerance test, insulin response test, serum creatinine test and adiponectin assay (ELISA) were carried out. Data was analysed using one way ANOVA and expressed as mean± standard error of mean (SEM) with p ≤ 0.05 considered as significant. L-arginine induced rapid insulin-like action which was effective after thirty minutes of oral glucose loading when compared the control group. Glucose uptake from the blood was also more effective and quicker in the L-arginine treated groups. Adiponectin was significantly expressed across the test groups when compared to the control group and there was insulin resistance in the untreated kidney injured rats 1 hour into the insulin response test. It may be concluded that L-arginine has a homeostatic influence on glucose handling in kidney-damaged rats possibly mediated by increased adiponectin expression.