Fiche publication
Date publication
octobre 2022
Journal
International journal of molecular sciences
Auteurs
Membres identifiés du Cancéropôle Est :
Dr LAGROST Laurent
,
Dr PAIS DE BARROS Jean-Paul
,
Pr MASSON David
Tous les auteurs :
Lebrun LJ, Pallot G, Nguyen M, Tavernier A, Dusuel A, Pilot T, Deckert V, Dugail I, Le Guern N, Pais De Barros JP, Benkhaled A, Choubley H, Lagrost L, Masson D, Gautier T, Grober J
Lien Pubmed
Résumé
Bacterial lipopolysaccharides (LPS, endotoxins) are found in high amounts in the gut lumen. LPS can cross the gut barrier and pass into the blood (endotoxemia), leading to low-grade inflammation, a common scheme in metabolic diseases. Phospholipid transfer protein (PLTP) can transfer circulating LPS to plasma lipoproteins, thereby promoting its detoxification. However, the impact of PLTP on the metabolic fate and biological effects of gut-derived LPS is unknown. This study aimed to investigate the influence of PLTP on low-grade inflammation, obesity and insulin resistance in relationship with LPS intestinal translocation and metabolic endotoxemia. Wild-type (WT) mice were compared with -deficient mice (-KO) after a 4-month high-fat (HF) diet or oral administration of labeled LPS. On a HF diet, -KO mice showed increased weight gain, adiposity, insulin resistance, lipid abnormalities and inflammation, together with a higher exposure to endotoxemia compared to WT mice. After oral administration of LPS, PLTP deficiency led to increased intestinal translocation and decreased association of LPS to lipoproteins, together with an altered catabolism of triglyceride-rich lipoproteins (TRL). Our results show that PLTP, by modulating the intestinal translocation of LPS and plasma processing of TRL-bound LPS, has a major impact on low-grade inflammation and the onset of diet-induced metabolic disorders.
Mots clés
LPS (lipopolysaccharides), PLTP (phospholipid transfer protein), dietary fat, inflammation, lipid metabolism, obesity
Référence
Int J Mol Sci. 2022 10 30;23(21):
