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Clinical evidence supporting the anti-inflammatory effects of GLP-1 receptor agonists comes primarily from cardiovascular outcome trials and mechanistic studies, though most research has examined standard therapeutic doses rather than specifically low-dose regimens
Anti-IAPP monoclonal antibody improves clinical symptoms in a mouse model of type 2 diabetes
The direct action of GIP on its receptor, which is expressed by these cells, is what causes GIP stimulation to increase glucagon secretion by alpha cells in contrast to GLP- 1 [72,73,74]
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However, while Glp1r is not expressed appreciably in mouse cardiomyocytes, some human ventricular and atrial cardiomyocytes do express GLP1R (40, 57)
