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I have not delved into this, but I wonder if Type I Diabetes is not an entirely different physiological environment, and therefore any findings in this context translate on a cellular level to T2DM or non-diabetic settings. TGR5 receptors might act differently on cAMP-PKA signalling. Or some other factors impacting insulin production. I wish this was in more common T2DM as that would be more relevant to prediabetics. But not being Type I, I suspend judgement.