Real world effectiveness of subcutaneous semaglutide in type 2 diabetes: A retrospective, cohort study (Sema-MiDiab01)

IntroductionAim of the present study was to evaluate the real-world impact of once-weekly (OW) subcutaneous semaglutide on different end-points indicative of metabolic control, cardiovascular risk factors, and beta-cell function in type 2 diabetes (T2D). MethodsThis was a retrospective, observational study conducted in 5 diabetes clinics in Italy. Changes in HbA1c, fasting blood glucose (FBG), body weight, blood pressure, lipid profile, renal function, and beta-cell function (HOMA-B) during 12 months were evaluated. ResultsOverall, 594 patients (97% GLP-1RA naive) were identified (mean age 63.9 +/- 9.5 years, 58.7% men, diabetes duration 11.4 +/- 8.0 years). After 6 months of treatment with OW semaglutide, HbA1c levels were reduced by 0.90%, FBG by 26 mg/dl, and body weight by 3.43 kg. Systolic blood pressure, total and LDL-cholesterol significantly improved. Benefits were sustained at 12 months. Renal safety was documented. HOMA-B increased from 40.2% to 57.8% after 6 months (p<0.0001). DiscussionThe study highlighted benefits of semaglutide on metabolic control, multiple CV risk factors, and renal safety in the real-world. Semaglutide seems to be an advisable option for preservation of beta-cell function and early evidence suggests it might have a role in modifying insulin resistance (HOMA-IR), the pathogenetic basis of prediabetes and T2D.

Automated summary

The aim of this study was to evaluate the real-world impact of once-weekly subcutaneous semaglutide on various aspects of metabolic control, cardiovascular risk factors, and beta-cell function in patients with type 2 diabetes. The results showed that after 6 months of treatment, semaglutide led to significant improvements in HbA1c levels, fasting blood glucose, body weight, blood pressure, and lipid profile. The study also demonstrated the renal safety of semaglutide and its potential role in preserving beta-cell function and modifying insulin resistance.