This pathophysiology diagram illustrates the hypothetical central and peripheral mechanisms of Liraglutide, a GLP-1 receptor agonist, in the context of Beckwith-Wiedemann Syndrome (BWS). The upper section shows a sagittal anatomical diagram of the human brain, highlighting the mesolimbic and homeostatic pathways involving the Nucleus Accumbens (NAc), Hypothalamus (HYP), and Ventral Tegmental Area (VTA), interconnected by blue neural pathways. Arrows from Liraglutide point to these regions, indicating a regulatory effect on food intake, reward, and hedonic feeding, potentially counteracting CDKN1C-related dopaminergic alterations. The lower section depicts the peripheral effect on adipose tissue. Liraglutide is shown stimulating a cluster of adipocytes, with positive signs (+) associated with preadipocyte differentiation, lipolytic markers, and IGF-2 expression. A detailed inset shows a single adipocyte expressing GLP-1R and IGF-2R receptors on its membrane, with IGF-2 acting as an extracellular ligand. This educational graphic demonstrates the drug's multi-organ approach to managing obesity by modulating central appetite signaling and peripheral lipid metabolism.

This pathophysiology diagram illustrates the comparative mechanisms of GLP-1 (glucagon-like peptide-1) action following bariatric surgery versus the administration of GLP-1 analogs. The bariatric surgery pathway is depicted as a gut-brain-periphery axis: surgery increases GLP-1 availability in the gut and portal vein, which is detected by hepatoportal sensors and afferent vagus nerve fibers. This signal travels to the brain for integration, which then sends efferent signals via vagal nerve fibers to trigger metabolic actions in peripheral organs like the pancreas. In contrast, the diagram shows GLP-1 analogs bypassing the gut-brain circuit to act directly on GLP-1 canonical receptors (represented by 7-transmembrane G protein-coupled receptor icons) located in tissues such as the brain and pancreas. Key anatomical landmarks included are the brain and the pancreas. This visual serves as an educational tool for endocrinology and metabolic surgery, highlighting the neuro-hormonal integration involved in endogenous GLP-1 signaling compared to direct pharmacological receptor activation.

This medical illustration depicts the sagittal view of the human brain, focusing on the neurocircuitry of appetite and reward in the hypothalamus and ventral tegmental area (VTA). The diagram illustrates the mechanism of action for various antiobesity medications. In the magnified hypothalamus section (arcuate nucleus, ARC), orexigenic NPY/AgRP neurons and anorexigenic POMC/CART neurons are shown. Liraglutide is depicted acting on GLP-1 receptors (GLP-1R) on both GABAergic and POMC/CART neurons. Lorcaserin targets the 5-HT2C receptor, while Naltrexone blocks the μ-opioid receptor (μ-OR) to prevent feedback inhibition. Topiramate is shown interacting with GABAergic neurons. The lower magnified section highlights the reward system, where Phentermine and Bupropion influence dopaminergic signaling in the VTA and nucleus accumbens. Key neurotransmitters involved include dopamine (acting on D1/D2 receptors), serotonin, and GABA. Arrows indicate excitatory and inhibitory pathways leading toward cortical reward centers, demonstrating the integration of homeostatic appetite control and hedonic reward processing.