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In diabetic kidney disease, mTORC1 hyperactivation is associated with kidney dysfunction and increased fibrosis.43 In a mouse model of non-proteinuric diabetic kidney disease, SGLT2i, particularly empagliflozin conferred renal protection by increasing endogenous ketones and suppressing mTORC1 activation in the kidneys.36 The treatment with empagliflozin mirrored the effect of exogenous ketone supplementation, where both treatments reduced kidney damage as evident through lower plasma cystatin-C levels and decreased interstitial fibrosis.36 The renoprotective mechanism of SGLT2i hinges on the ketogenesis rate-limiting enzyme HMGCS2 highlighting ketone productions central role in its antifibrotic effects.36 51 Antioxidative effects Ketones, specifically BHB, act as an important signaling molecule influencing gene expression through various regulatory pathways
Injection sites must be shifted each week to avoid skin irritation between the abdomen, upper thigh, or the backs of the upper arms
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