L-arginine mitigates cardiac lipid and glucose accumulation through leptin modulation and enhancement of PIK3 activities in high fat-fed male Wistar rats.

Abstract

Background and aim: Insulin resistance and other metabolic risk factors are associated with increased cardiovascular diseases in animals fed with high fat diets (HFD). L-arginine is a semi-essential amino acid produced both endogenously and taken in the diet as supplements. It has been documented to possess antioxidant and anti-inflammatory properties and has been considered a plausible candidate for the management of metabolic disorders. Therefore, this study is aimed to determine the effects of L-arginine on lipid dysregulation and insulin resistance in high fat-fed male Wistar rats.

Methods and results: Twenty-four (24) male Wistar rats randomly selected into 4 groups, mean weight 110 ± 5 and, (n = 6) were fed rat chow + distilled water (vehicle); CTR, rat chow + L-arginine (150 mg/kg), HFD + vehicle, HFD + L-Arginine (150 mg/kg) for 6 weeks. The animals were anesthetized with 50 mg/kg pentobarbital sodium intraperitoneally, blood sample was taken via cardiac puncture and thereafter collected into a heparinized tube. Data were expressed as means ± SEM. HFD increased body weight gain, serum Insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), area under the curve (AUC), leptin, Lipoprotein(a) or Lp(a), triglyceride-glucose index (TYG), triglycerides (TG), free fatty acids (FFAs), total cholesterol (TC), low density lipoprotein (LDL-C), TC/HDL-C, Log TG/HDL-C, TC-HDL-C)/HDL-C but decreased phospoinositide-3-kinase (PIK3) when compared with control. L-arginine, resulted in significant reduction in weight gain, fasting blood sugar (FBS), insulin, AUC, HOMA-IR, leptin, while increasing PIK3, Lp(a), TG, TC and FFA when compared with HFD.

Conclusion: The amelioration of lipid and glucose accumulation by L-arginine supplementation in high fat diet-fed male Wistar rats is accompanied by reduced leptin levels and PIK3 augmentation.