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Lipopolysaccharide binding protein resists hepatic oxidative stress by regulating lipid droplet homeostasis. | LitMetric

AI Article Synopsis

  • Oxidative stress causes lipid accumulation by affecting lipid droplet (LD) homeostasis, where lipid droplets store unsaturated triglycerides to protect them from damage.
  • The study identifies lipopolysaccharide-binding protein (LBP) as a key player that increases lipid storage in LDs by capturing unsaturated triglycerides and helping to manage lipid-redox balance under oxidative stress.
  • Chronic stress raises LBP levels, contributing to conditions like insulin resistance and obesity, highlighting LBP's potential as a target for therapies aimed at reducing oxidative stress-related metabolic issues.

Article Abstract

Oxidative stress-induced lipid accumulation is mediated by lipid droplets (LDs) homeostasis, which sequester vulnerable unsaturated triglycerides into LDs to prevent further peroxidation. Here we identify the upregulation of lipopolysaccharide-binding protein (LBP) and its trafficking through LDs as a mechanism for modulating LD homeostasis in response to oxidative stress. Our results suggest that LBP induces lipid accumulation by controlling lipid-redox homeostasis through its lipid-capture activity, sorting unsaturated triglycerides into LDs. N-acetyl-L-cysteine treatment reduces LBP-mediated triglycerides accumulation by phospholipid/triglycerides competition and Peroxiredoxin 4, a redox state sensor of LBP that regulates the shuttle of LBP from LDs. Furthermore, chronic stress upregulates LBP expression, leading to insulin resistance and obesity. Our findings contribute to the understanding of the role of LBP in regulating LD homeostasis and against cellular peroxidative injury. These insights could inform the development of redox-based therapies for alleviating oxidative stress-induced metabolic dysfunction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11016120PMC
http://dx.doi.org/10.1038/s41467-024-47553-5DOI Listing

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