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Similarly, in mesangial cells, GLP-1 receptor agonists have been shown to suppress either high-glucose-induced or AGEs-induced pro-fibrotic signalling pathways, including NF-B activation and TGF-1 expression, leading to reduced ECM deposition [60,61], and to suppress their proliferation via AMPK activation [62]

Thats especially true with weekly GLP1 injections, where timing affects how the medication builds up and tapers off throughout the week

Animal offspring exposed to spironolactone during late pregnancy exhibited changes in the reproductive tract, including dose-dependent decreases in weights of the ventral prostate and seminal vesicle in males, ovaries and uteri that were enlarged in females, and other indications of endocrine dysfunction that persisted into adulthood

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MOTS-c activates AMPK through the AICAR accumulation pathway described earlier

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