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The distribution map of SEMA in the central nervous system shows a greater presence in the septal nuclei compared to LIRA.19 In addition to reducing food intake, SEMA has proven effective in modulating food preferences,12 likely through dopaminergic activation of the ventral tegmental area and a reduction in endocannabinoid tone.19 The subsequent activation of the parabrachial nucleus and other neural circuits involved in the hedonic regulation of food intake may be specific to SEMA, potentially helping to explain its differences from LIRA.19 The mechanisms involved in the improvement of glycaemic control by LIRA 3 mg and SEMA 2.4 mg are related to their incretin and glucagonostatic effects inherent to GLP-1 receptor agonism,3 as well as to those derived from weight loss, reduction in fat mass, and their associated consequences.20 Effects on other comorbidities The SCALE programme shows that the apnoea-hypopnoea index reduces in cases of sleep apnoea syndrome when LIRA is used instead of a placebo (12.2 vs 6.1, p = 0.015).21 The contribution of weight loss to the effects of LIRA treatment in the SCALE programme varies
