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GLP-1 delays gastric emptying via stimulating inhibitory nitrergic myenteric neurons [18] and activating vagal afferents [19], leading to reduced gastrointestinal motility [20]

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By uncoupling oxidative phosphorylation from ATP synthesis, they increase energy expenditure and improve metabolic parameters, making them promising candidates for treating diseases characterized by nutrient excess and metabolic dysfunction (9-11,17)

Neuroinflammation, vascular dysfunction, and cellular dysfunction regarding astrocytes and neurons have been discussed as underlying mechanisms contributing to these structural and functional alterations [94]

Similar to skeletal muscle, carnitine supplementation increased most acyl-carnitine species in adipose tissue (Fig