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/HDLC, 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.