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At the cellular level, the effects of excess soluble urate include perturbation of nitric oxide metabolism [11] and of the renin-angiotensin axis [12], promotion of insulin resistance mediated partly via inhibition of hepatic AMP-activated protein kinase (AMPK) [13], and a role in nonalcoholic steatohepatitis (NASH) through the stimulation of lipogenesis and the inhibition of fatty acid (FA) oxidation [14,15,16,17]

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In our studies, antagonizing the GIPR did not affect tirzepatide-stimulated insulin secretion or glycemic control during an IPGTT at doses of 3 nmol kg 1 , which we identified as maximal for glucose lowering in mice

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