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Randomized Controlled Trial
. 2024 Aug 1;47(8):1350-1359.
doi: 10.2337/dc24-0491.

Effect of Semaglutide on Regression and Progression of Glycemia in People With Overweight or Obesity but Without Diabetes in the SELECT Trial

Steven E Kahn  1 , John E Deanfield  2 , Ole Kleist Jeppesen  3 , Scott S Emerson  4 , Trine Welløv Boesgaard  3 , Helen M Colhoun  5 , Robert F Kushner  6 , Ildiko Lingvay  7 , Bartolome Burguera  8 , Grzegorz Gajos  9 , Deborah Bade Horn  10 , Irene M Hramiak  11 , Ania M Jastreboff  12 , Alexander Kokkinos  13 , Michael Maeng  14 , Ana Laura S A Matos  3 , Francisco J Tinahones  15 , A Michael Lincoff  16 , Donna H Ryan  1   17 ; SELECT Trial Investigators
Affiliations
Randomized Controlled Trial

Effect of Semaglutide on Regression and Progression of Glycemia in People With Overweight or Obesity but Without Diabetes in the SELECT Trial

Steven E Kahn et al. Diabetes Care. .

Abstract

Objective: To determine whether semaglutide slows progression of glycemia in people with cardiovascular disease and overweight or obesity but without diabetes.

Research design and methods: In a multicenter, double-blind trial, participants aged ≥45 years, with BMI ≥27 kg/m2, and with preexisting cardiovascular disease but without diabetes (HbA1c <6.5%) were randomized to receive subcutaneous semaglutide (2.4 mg weekly) or placebo. Major glycemic outcomes were HbA1c and proportions achieving biochemical normoglycemia (HbA1c <5.7%) and progressing to biochemical diabetes (HbA1c ≥6.5%).

Results: Of 17,604 participants, 8,803 were assigned to semaglutide and 8,801 to placebo. Mean ± SD intervention exposure was 152 ± 56 weeks and follow-up 176 ± 40 weeks. In both treatment arms mean nadir HbA1c for participants was at 20 weeks. Thereafter, HbA1c increased similarly in both arms, with a mean difference of -0.32 percentage points (95% CI -0.33 to -0.30; -3.49 mmol/mol [-3.66 to -3.32]) and with the difference favoring semaglutide throughout the study (P < 0.0001). Body weight plateaued at 65 weeks and was 8.9% lower with semaglutide. At week 156, a greater proportion treated with semaglutide were normoglycemic (69.5% vs. 35.8%; P < 0.0001) and a smaller proportion had biochemical diabetes by week 156 (1.5% vs. 6.9%; P < 0.0001). The number needed to treat was 18.5 to prevent a case of diabetes. Both regression and progression were dependent on glycemia at baseline, with the magnitude of weight reduction important in mediating 24.5% of progression and 27.1% of regression.

Conclusions: In people with preexisting cardiovascular disease and overweight or obesity but without diabetes, long-term semaglutide increases regression to biochemical normoglycemia and reduces progression to biochemical diabetes but does not slow glycemic progression over time.

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