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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Haines noted that it is still unclear which patients are most likely to lose muscle and how this muscle loss might impact blood sugar control
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