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LBP resists hepatic oxidative stress by regulating LD homeostasis

ABSTRACT: we explored the novel role of Lipopolysaccharide-binding protein (LBP) as an anti-oxidant, which can capture unsaturated triglyceride (TG) into LDs to avoid lipid peroxidation. Oxidative stress upregulates LBP level and promotes LDs growth via the LBP/TG phase transition. Upon N-Acetyl-L-cysteine (NAC) elimination of ROS, LBP is exported from LD along with PRDX4, resulting in an increase in phospholipid synthesis. Chronic stress causes LBP upregulation and leads to obesity, which can be rescued by NAC treatment in vivo. These results support that LBP maintains homeostasis by coupling lipid metabolism and redox signal, which provides insights into redox medicine that mitigate stress-induced metabolic dysfunction.

INSTRUMENT(S): Orbitrap Exploris 480, Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hepatocyte, Liver

SUBMITTER: Qilun Zhang

LAB HEAD: Qilun Zhang

PROVIDER: PXD040940 | Pride | 2024-04-10

REPOSITORIES: Pride

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