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New research uncovers how a natural polyamine, spermidine, modifies RIPK1 to block inflammation and metabolic damage, opening doors to innovative diabetes treatments. Image Credit: Ti_A / Shutterstock In a recent study published in the journal Nature Cell Biology , researchers investigated how N-acetyltransferase (NAT)-mediated post-translational modification, acetylhypusination, regulates insulin sensitivity and necroptosis. Type 2 diabetes (T2D) is a significant global health concern, with over 537 million adults affected.

Current T2D management approaches mainly focus on regulating hyperglycemia, which is believed to be implicated in progressive tissue/organ damage observed in the end stages of T2D. Nevertheless, the mechanisms underlying T2D onset and progression are poorly understood. Role in Longevity: Spermidine is recognized as a longevity agent due to its ability to induce autophagy, reduce inflammation, and regulate lipid metabolism, contributing to extended lifespan in model organisms and improved cellular health in humans.



The gene encoding human NAT2 (hNAT2), an ortholog of murine Nat1 (mNAT1), has been reported to mediate insulin sensitivity. hNAT2 and mNAT1 serve as arylamine N-acetyltransferases in the xenobiotic metabolism of exogenous molecules, like aliphatic amines and some drugs. Recent studies indicate that NAT2 acetylates endogenous aliphatic amines, such as spermidine and putrescine.

Spermidine is a natural polyamine found in cells whose post-translati.

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