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We show that the cardioprotective actions of GLP-1(2836) do not depend on a functional transmembrane GLP-1R but rather are mediated intracellularly through type 10 soluble adenylyl cyclase (sAC), accompanied by increased cAMP levels, protein kinase A (PKA) activation, and endothelial nitric oxide synthase (eNOS) phosphorylation

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But like most powerful tools they come with a few trade-offs worth understanding, like a potentially higher risk of osteoporosis, a condition where bones become weaker and more likely to break

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