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However, in diseased kidneys, mitochondrial dysfunction has been reported as a key pathologic feature that contributes to disease initiation and progression.29 30 For example, in diabetic nephropathy (DN), hyperglycemia-induced flux of glycolysis increases oxygen demand with the by-product of amplified ROS.30 31 Excess glucose use in the kidney shifts the energy reliance from fatty acid metabolism to glycolysis, even in the proximal tubules.30 31 The renoprotective effect of SGLT2i in diabetic kidney disease is driven by amelioration of the pathologic metabolic shift from FAO to glycolysis

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In addition, Tirzepatide also binds to GIP receptors on -cells to co-stimulate insulin secretion by upregulating intracellular cAMP levels via GPCR-signaling

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