Effect of saroglitazar in South Indian patients with diabetic dyslipidemia uncontrolled on a moderate-intensity statin and the association of PPAR α and γ gene polymorphisms with its response

Isaac J. Bage; Sadishkumar Kamalanathan; Sandhiya Selvarajan; Jayaprakash Sahoo; Jayanthi Mathaiyan; Dukhabandhu Naik

doi:10.18203/2319-2003.ijbcp20231121

Authors

Isaac J. Bage Department of Endocrinology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Sadishkumar Kamalanathan Department of Endocrinology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Sandhiya Selvarajan Department of Clinical Pharmacology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Jayaprakash Sahoo Department of Endocrinology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Jayanthi Mathaiyan Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India
Dukhabandhu Naik Department of Endocrinology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India

DOI:

https://doi.org/10.18203/2319-2003.ijbcp20231121

Keywords:

Diabetic dyslipidemia, PPARα/γ agonist, Single nucleotide polymorphisms, Saroglitazar

Abstract

Background: Diabetic dyslipidemia is associated with atherosclerosis risk factors and cardiovascular disease. Saroglitazar is a dual PPAR α and γ agonist approved initially for diabetic dyslipidemia and later for managing non-alcoholic steatohepatitis and hyperglycemia in T2DM. This study was conducted to estimate the association of studied PPAR α and γ gene polymorphisms among patients with diabetic dyslipidemia at baseline and with triglyceride response to saroglitazar administration.

Methods: A total of 54 diabetic dyslipidemia patients who are not controlled i.e., triglycerides (TG)>200 mg/dl with moderate intensity of atorvastatin (≥10 mg) were recruited to the study. All the patients were given saroglitazar 4 mg once daily for 12 weeks. PPARα single nucleotide polymorphisms (SNPs) rs1800206, rs4253778, rs135542 and those of PPARγ gene rs3856806, rs10865710, rs1805192 were genotyped by real-time PCR.

Results: 54 patients (67% female) with a mean age of 48.01±6.73 years were given saroglitazar 4 mg once daily for 12 weeks. There was a significant decrease in TG (36.9%) from baseline of 292.33±83.81mg/dl (mean±SD) to 184.46±95.90 mg/dl (<0.001) and in HbA1c (0.66%) from baseline of 8.5% to 7.8% (<0.001). PPAR α and PPAR γ gene variants did not show any association with TG lowering response.

Conclusions: Saroglitazar 4mg once daily effectively decreases the TG, non-HDL-C levels, and HbA1c with no major adverse events, and TG lowering response is not associated with the studied polymorphisms.

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