Dyslipidemia is a common feature of diabetes. A characteristic pattern, termed Diabetic dyslipidemia (DD) characterized by elevated fasting and postprandial glucose along with triglycerides (TG; >1.7mmol/L), low HDL-cholesterol (HDL-C;<1.3mmo/L in F, <1.0mmol/L in M), elevated/normal LDL-cholesterol (LDL-C; >3.0mmol/L) and with the predominance of small dense LDL particles. In diabetic dyslipidemia, insulin resistance facilitates the increase of free fatty acid (FFA) flux. The increased FFA level boosts TG and VLDL production as well as triggers oxidative stress and lipid peroxidation, all of which closely associated with the development of NAFLD.

 The criteria for the definition of NAFLD requires that (a) there is evidence of hepatic steatosis, either by imaging or by histology and (b) there are no causes for subsequent hepatic fat accumulation such as significant alcohol consumption, use of steatogenic medication or hereditary disorders. NAFLD can be categorized histologically into the nonalcoholic fatty liver (NAFL: the presence of ≥5% hepatic steatosis without evidence of hepatocellular injury in the form of hepatocyte ballooning) or nonalcoholic steatohepatitis (NASH: the presence of ≥5% hepatic steatosis and inflammation with hepatocyte injury (e.g., ballooning), with or without any fibrosis). Regarding dyslipidemia as the plausible link for NAFLD, aggressive management of dyslipidemia and prevention may represent a promising addition to the treatment of NAFLD. Thus, the ideal therapeutic strategy for NAFLD management should not only reverse the excessive lipid accumulation in hepatocytes but also attenuate the hepatic inflammatory reaction, endothelial dysfunction, and insulin resistance in the liver, eventually preventing the progression of simple steatosis to NASH.

 Saroglitazar is a dual peroxisome proliferator-activated receptor (PPAR) agonist indicated for the treatment of hypertriglyceridemia in Type II diabetics by Drug Controller General of India (DCGI) in June 2013, and also various studies showed its efficacy in improving NAFLD. Ranolazine approved as an antianginal agent in January 2006, but post hoc analyses of various angina trials (like MERLIN-TIMI 36 Randomized control trial) suggested the drug ability to lower HbA_1c, and in addition to this, the preliminary studies suggest that ranolazine treatment reverses obesity-induced NAFLD. Different class of drugs with the same actions in mitigating NAFLD brought to this comparative study.

              To our knowledge, this study works to adds a new indication for ranolazine in the treatment of NAFLD. Our current work aims to compare the associations of the (Nonalcoholic fatty liver disease) NAFLD with Type ΙΙ Diabetes Mellitus and dyslipidemia (DL). The factors associated with Type 2 DM, DL, NAFLD are to be analyzed. Also, the safety of both drugs (Ranolazine and Saroglitazar) are compared on NAFLD in diabetes dyslipidemic patients. The efficacies of both the drugs in lowering the lipid profile and glucose levels will be monitored.

             This study investigates biomarkers for glycemic control (hemoglobin A_1c and random blood glucose, insulin), lipid metabolism (triglycerides, total cholesterol, high-density lipoprotein [HDL], and low-density lipoprotein [LDL]), albumin, and hepatic cholestasis (gamma-glutamyl transferase [GGT]) in NAFLD. Its mean purpose was to determine whether these biomarkers could detect improvement in progression of NAFLD in Diabetic dyslipidemic patients receiving Ranolazine and Saroglitazar.