Study reveals how high glucose triggers cognitive decline via HSD17B10 lactylation and lipid droplet accumulation in neurons
By
Tianpeng Zheng1,2,3,8 Send email to [email protected]
Summary
This study by Xu et al. investigates how high glucose impairs cognitive function in type 2 diabetes. Using lactylome analysis, the researchers demonstrate that high glucose induces lactylation of the HSD17B10 enzyme at the K105 site in hippocampal neurons, mediated by the lactyltransferase Aars1. This lactylation reduces HSD17B10 enzyme activity, leading to impaired breakdown and excessive accumulation of lipid droplets, which ultimately causes neuronal apoptosis and cognitive decline. The study also identifies a short peptide that competitively inhibits HSD17B10 K105 lactylation as a potential therapeutic approach for preventing and treating diabetes-associated cognitive impairment.
Source
bskyStudy reveals how high glucose triggers cognitive decline via HSD17B10 lactylation and lipid droplet accumulation in neuronscell.comKey quotes
· 3 pulledHigh glucose induces HSD17B10 K105 lactylation in hippocampal neurons by upregulating lactyltransferase Aars1, which reduces HSD17B10 enzyme activity
Impaired breakdown and excessive accumulation of lipid droplets... ultimately leading to neuronal apoptosis and cognitive decline
A short peptide that competitively inhibits HSD17B10 K105 lactylation [highlights] promising molecular targets for the prevention and treatment of diabetes-associated cognitive impairment
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