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Life sciences · Journal article
Endocrinology Diabetes & Metabolism · November 1, 2026
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ABSTRACT Introduction Metabolic dysfunction‐associated steatotic liver disease ( MASLD ) is the leading cause of chronic liver disease globally, driven by rising obesity and type 2 diabetes mellitus ( T2DM ). Existing medications provide minimal fibrosis regression, highlighting the need for comparative evidence on agents with metabolic and hepatic benefits. This study compared the efficacy and safety of saroglitazar 4 mg and dapagliflozin 10 mg in patients with MASLD. Methods This 25‐week, prospective, multicentre, open‐label active‐controlled comparative cohort study enrolled adults aged 18–70 years with MASLD confirmed by FibroScan (steatosis grade S3, controlled attenuation parameter [ CAP ] ≥ 292 dB /m, and/or fibrosis stage ≥ F2, liver stiffness measurement [ LSM ] ≥ 8.0 kPa ). Participants received saroglitazar ( n = 27) or dapagliflozin ( n = 27) once daily, added to standard of care per physician discretion. The primary endpoint was change from baseline in hepatic steatosis ( CAP ) and fibrosis ( LSM ); secondary endpoints included HbA1c, hepatic enzymes, lipid profile, and adverse events. Results All 54 participants completed follow‐up. CAP decreased from 314.7 to 278.7 dB /m with saroglitazar and from 310.2 to 287.0 dB /m with dapagliflozin (between‐group p = 0.44). LSM decreased in both arms (saroglitazar −0.96 kPa; dapagliflozin −0.46 kPa; between‐group p = 0.80). HbA1c improved in both groups (saroglitazar 8.28%–6.76%; dapagliflozin 8.14%–7.30%), with a significantly greater reduction with saroglitazar (between‐group p = 0.04). ALT and AST declined similarly in both arms despite higher baseline ALT with saroglitazar. Triglycerides decreased significantly within both groups (saroglitazar −62.5 mg/ dL; dapagliflozin −28.3 mg/ dL ), with no significant between‐group difference. No treatment‐emergent adverse events, including edema, occurred in either group. Conclusions Both saroglitazar and dapagliflozin improved hepatic steatosis, fibrosis markers, liver enzymes, and glycemic control over 25 weeks, with comparable hepatic benefit. Saroglitazar produced a significantly greater reduction in HbA1c, suggesting a possible glycemic‐preferential advantage in patients requiring simultaneous glycemic and hepatic control; larger randomized trials are needed to confirm any differential hepatic efficacy. Trial Registration Clinical Trials Registry of India, CTRI /2024/08/071848