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This centrally produced GLP-1 reaches specific receptors located in key structures involved in appetite regulation, such as the paraventricular nucleus, the lateral septum, the nucleus accumbens and the lateral parabrachial nucleus.2,3,6 Furthermore, it promotes aversive responses, inhibits neuroinflammation and gastric emptying, and stimulates sympathetic tone and thermogenesis in experimental models.2,4,6 Activation of GLP-1R on neurons in the arcuate nucleus stimulates the production of pro-opiomelanocortin (POMC), which in turn inhibits neurons that produce neuropeptide Y (NPY), thereby generating an appetite-suppressing response.2 GLP-1 production has also been reported in the olfactory bulb, although its significance remains unclear.2,6 GLP-1R has been identified in the sinoatrial node, atrial and ventricular myocytes, and vascular endothelium
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This is because: GLP-1 agonists: Slow gastric emptying, enhance insulin secretion, regulate hepatic glucose Amylin agonists: Suppress appetite centrally, slow gastric emptying via distinct pathways Together: Complementary mechanisms produce additive/synergistic effects on weight loss Cagrilintide Monotherapy Trials Initial clinical development focused on establishing the safety, tolerability, and efficacy of cagrilintide as a standalone therapy for weight management
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These GLP-1 medications are revolutionizing obesity care but how soon can you expect to see results
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