NLRP3 Inflammasome Modulates Post-Burn Lipolysis and Hepatic Fat Infiltration via Fatty Acid Synthase.
Ontology highlight
ABSTRACT: Burns result in generalized catabolism, lipolysis, and hyperinflammation. NLRP3 inflammasome, a mediator of hyperinflammation, is upregulated in burn patients' adipose tissue within 7 days post-burn. However, its role during the acute phase is unknown. Here, wild-type (WT) and NLRP3 knockout (NLRP3-/-) mice were exposed to 25% TBSA scald burn. Flow cytometric analysis demonstrated greater liver macrophage infiltration in NLRP3-/- yet decreased protein expression of NLRP3 components, ER stress, and apoptosis. NLRP3-/- had increased circulating free fatty acids (FFA), fatty deposition and liver weight 1 hour post-burn. Alterations in adipose fatty acid synthase (Fasn) expression affects FFA levels post-burn; WT have an early peak in Fasn gene and protein expr
SUBMITTER: Vinaik R
PROVIDER: S-EPMC6185951 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature
ACCESS DATA