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By far the most unexpected result of the present study is the defect in cAMP generation that we have measured downstream of GLP-1 stimulation for the triple AA phospho-null mutant compared to the WT receptor in our -cell system
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Osama Z
On the other hand, in kidneys, the activation of GLP1-R without receptors, sited in the proximal tubule and pre-glomerular portion, increases cAMP levels, which then triggers PKA activity, inhibiting oxidative renal injury and thus delaying the development of diabetic nephropathy
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While the effect is modest and transient, it represents another natural lever for supporting GLP-1 levels
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