Diabetes mellitus is one of the most common chronic diseases globally responsible for increased morbidity and mortality. The global prevalence of diabetes among adults is estimated to be 6.4%, affecting 285 million people, in 2010, and is expected to increase to 7.7%, affecting 439 million people by 2030. Between 2010 and 2030, it is estimated that there will be a 69% and 20% increase in number of adults with diabetes in developing countries and developed countries, respectively. Diabetes has evolved into an epidemic in India. The estimated number of patients with diabetes in India was 62.4 million in 2011 which is projected to rise to a staggering 101.2 million by 2030.

Patients with Type 2 diabetes mellitus are associated with a considerably increased risk of premature atherosclerosis, particularly coronary heart disease (CHD) and peripheral arterial disease, which is the leading cause of death in these individuals. Epidemiologic studies have demonstrated that diabetes mellitus is an independent risk factor for cardiovascular disease. The mortality associated with a coronary event in people with diabetes mellitus is significantly higher than the mortality in nondiabetic individuals.

Diabetic Dyslipidaemia (DD) consists of specifically mild to marked elevation of triglyceride rich lipoproteins- very low density lipoprotein-cholesterol (VLDL-C) and VLDL-C remnants, and low levels of high density lipoprotein-cholesterol (HDL-C).In some patients with type 2 DM, dyslipidaemia may be a consequence of the deranged metabolic state of diabetes mellitus. i.e., hyperglycaemia and insulin resistance; in these patients, good control of hyperglycaemia might mitigate the dyslipidaemia. However, since ideal glycaemic control generally is not possible in most patients with type 2 DM, some degree of dyslipidaemia often persists regardless of attempts to normalize plasma glucose levels. Even after effective control of hyperglycaemia has been achieved, insulin resistance may not improve and may contribute to dyslipidaemia

Diabetes-related changes in plasma lipid levels are among the key factors that are amenable to intervention. Existing therapy for the management of hypertriglyceridemia is lifestyle changes and pharmacotherapy with statins alone or in combination with fibrates, niacin, omega-3 fatty acids, cholesterol absorption inhibitor.  At high doses, statins may cause severe adverse effect in the form of myotoxicity, myopathy, myalgia, myositis or rhabdomyolysis. Statin toxicity is usually observed as myalgia or muscle weakness with creatine kinase (CK) levels greater than 10 times the normal upper limit. Rhabdomyolysis is the most severe adverse effect of statins, which may result in acute renal failure, disseminated intravascular coagulation and death. Hepatic function is also known to be affected by statin use.  

Recent data also suggests that statin therapy for long term, especially in high dose can worsen the glycaemic control and can lead to new onset of T2DM. Fibrates can also cause myopathy, occurring at a rate similar to that of statin therapy. The risk for myopathy appears to be elevated in patients with combination therapy with statins and renal dysfunction, hence fibrates should be avoided in populations with severe renal impairment.

Saroglitazar has dual property of treating hypertriglyceridemia primarily and have some effect on hyperglycemia also. Saroglitazar is a dual PPAR-α/γ agonist. It has strong PPAR- α action with moderate PPAR-γ action. Myopathy as adverse effect is not documented with Saroglitazar. It is approved for treatment of diabetic dyslipidemia as add on therapy with statins. This study is proposed with the hypothesis that Saroglitazar may act as better alternative to fibrates as add on therapy to statins in the treatment of diabetic dyslipidemia.