The risks and rewards of semaglutide in obesity treatment

The connection between the pancreas, the gut and incretins – hormones released into the blood by the intestine in response to food – was established in the early twentieth century (Knudsen and Lau, 2019). With the incretin hormone glucagon-like peptide-1 (GLP-1) shown to account for up to 70% of insulin secretion in response to nutrient intake, its therapeutic potential in type 2 diabetes (T2D) was realised, leading to the development of semaglutide, which mimics GLP-1 by promoting insulin release and reducing the blood concentration of glucose (Knudsen and Lau, 2019).

Although semaglutide has been used in the treatment of T2D, Wilding et al (2021) reported the results of a double-blind trial of 1961 non-diabetic adults with a body-mass index (BMI) of 30 or greater, randomly assigned ‘to 68 weeks of treatment with once-weekly subcutaneous semaglutide (at a dose of 2.4 mg) or placebo, plus lifestyle intervention’. They found that obese or overweight non-diabetic adults ‘had a mean weight loss of 14.9% from baseline with semaglutide as an adjunct to lifestyle intervention. This loss exceeded that with placebo plus lifestyle intervention by 12.4 percentage points’ (Wilding et al, 2021).