In addition to acting through the p38 pathway, GLP-1RAs also promote the increase of PKA levels via the cAMP-dependent pathway, which in turn prevents the phosphorylation of epidermal growth factor receptor (EGFR) and activator of transcription 3 (STAT3), resulting in the inactivation of the EGFR-STAT3 signaling pathway in tumor cells and subsequently downregulating several downstream effector genes such as myelocytomatosis oncogene (c-Myc), survivin, cyclin D1, Bcl-xl, and Bcl-2, thereby inducing apoptosis in tumor cells in a dose-dependent manner [70, 73]
The glucagon receptor component should increase resting energy expenditure
[DOI] [PubMed] [Google Scholar] 71.Wang M., Xu R., Liu X., Zhang L., Qiu S., Lu Y., Zhang P., Yan M., Zhu J
doi: 10.1677/ERC-09-0087 4 Aschebrook-KilfoyBSabraMMBrennerAMooreSCRonESchatzkinAet al
Glucagon does something neither GLP-1 nor GIP can do: it increases energy expenditure
But the timing matters for accurate baseline and follow-up comparisons