Specific mutations in genes controlling GLP-1 receptor signaling, appetite regulation, and fat metabolism influence baseline sensitivity to these drugs
GLP-1Rs are expressed in the pancreas, intestinal intraepithelial lymphocytes, myocardium, adipose tissue, kidney, liver, blood vessels, lungs and in the CNS.2,3 Although GLP-1 is known for its incretin effect, which it shares with glucose-dependent insulinotropic peptide (GIP), the intake-regulating action, essential for its efficacy against obesity, occurs through its interaction with receptors located in the CNS.1,5 The GLP-1 peptide can reach the central nervous system (CNS) via peripheral vagal afferents, which transmit its action through the nodose ganglion to the nucleus tactus solitarius (NTS)
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a survival plot for MOF on a non-matched dataset was also produced (44)
Effective biomarkers, such as GPX4, 4-HNE, and MDA in joint fluid, can be used to monitor treatment response and assist in dose optimization (Table 2)