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The seemingly obvious mechanism is probably too simplistic, but appears to be supported by the recent review paper quoted below: The exact pathophysiology of FQ-induced tendinopathy remains elusive

A straightforward explanation for effects in the NTS could be that stimulation of GLP1 autoreceptors in the NTS would be expected to reduce release of GLP1 to other brain regions, removing a tonic inhibitory modulation on reward/consummatory functions

Mice with TrxR1/Gsr-null livers are highly sensitive to pharmacological inhibition of GSH biosynthesis by buthionine sulfoximine (BSO

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Its dual incretin and glucagon activity may help improve sensitivity to insulin and glucose regulation