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Both semaglutide and tirzepatide have been subject to intermittent shortage designations, creating a legal framework for compounding
Montrose-Rafizadeh C, Avdonin P, Garant MJ, Rodgers BD, Kole S, Yang H, et al
First, GLP-1RAs have been shown to inhibit the expression and release of proinflammatory cytokines, such as IL-6 and TNF-, thereby inhibiting the overall inflammatory response.461 GLP-1RAs can suppress the activation of nuclear factor-kappa B (NF-B), a key transcription factor involved in the regulation of inflammatory processes.462 Inhibition of the NF-B signaling pathway leads to the decreased production of inflammatory mediators, including adhesion molecules and chemokines, which are crucial for the recruitment of immune cells to sites of inflammation.463 In addition, liraglutide can delay the formation of AS by inducing cell cycle arrest in vascular smooth muscle cells through the AMPK pathway.5 GLP-1RAs and hypertension The carotid body, a vital chemoreceptor in the human body, plays a pivotal role in the regulation of respiratory and cardiovascular activity, energy homeostasis, and blood glucose sensitivity.464 Notably, the carotid body expresses GLP-1R, which is implicated in the concurrent regulation of blood pressure and blood glucose.465 The downregulation of GLP-1R expression may represent a significant contributory factor to the co-occurrence of hypertension and hyperglycemia.466 One study proposed a novel mechanism wherein postprandial GLP-1 release, under normal physiological conditions, inhibits the activity of chemosensory cells in the carotid body, thereby counteracting sympathetic excitability mediated by elevated blood glucose or insulin levels.465 Impaired GLP-1 secretion or reduced GLP-1R expression may result in aberrantly heightened sympathetic excitation
