Endocrine Abstracts

Introduction: Type 2 diabetes, obesity and fatty liver disase are the most common comorbidities at the orgin of metabolic syndrome. Treatment of these conditions overlaps significantly. The most recent innovation in the armamentarium of pharmacotherapy of type 2 diabetes is Glp 1 agonist, More recent research on the effect of GLP-1 receptor agonist on weight loss, metabolic parameters and fatty liver disease are promising. The weight reduction offered by GLP-1 agonist treatment has significant impact on the progression of fatty liver. Semaglutide, a weekly GLP 1 agonist, is used to treat type 2 diabetes patient and more recently approved for the treatment of obesity in patient without type 2 diabetes. Newsome et al, have shown that ALT normalized in 25-48% subjects treated with semaglutide (1).

Rational: The rational of this study is to assess the improvement of hba1c, weight reduction and improvement in AST and ALT in type 2 diabetes patients treated with semaglutide.

Methods: 50 patients attending Endocrinology Clinic in Mediclinic Parkview Hospital and Mediclini Dubai mall and started on Semaglutide were followed. Hba1c, weight and AST ALT levels were recorded before and 6months and 12 months after starting semaglutide.

Results: Our sample included 50 treated subjects (43 male (86%), 7 female). While the medication did not show a significant reduction in ALT and AST levels in 6 months, semaglutide showed a significant reduction in weight in 6 months. 82% of the sample had an average of 5% percentage change reduction in weight from baseline to 12 months, with all 7 women having reduced on 11% average and men with 4% percentage reduction in weight. Semaglutide also had a significant relation with HbA1c, showing reduction at 6 months (-0.15 percentage points, P<0.001) as well as in 12 months (-0.14 percentage points, P<0.001).

Discussion: Our study have shown two established benefits of semaglutide, a reduction of hba1c and reduction of body weight. However it did not show a signficiant improvement in AST and ALT, one possible explanation is that the sample of patients did not have established fatty liver disease at baseline, they were also not followed for a long enough period of time to establish a significant relationship.