脂肪变性
渗透(HVAC)
内科学
内分泌学
巨噬细胞
脂肪变
医学
生物
脂肪肝
体外
遗传学
物理
疾病
热力学
作者
Ryota Tanida,Hisanori Goto,Hiroaki Takayama,Yujiro Nakano,Hein Ko Oo,Cynthia M. Galicia‐Medina,Kenta Takahashi,Kiyo‐aki Ishii,Arman Syah Goli,Takashi Matsuzaka,Kenichi Harada,Toshinari Takamura
出处
期刊:Endocrinology
[The Endocrine Society]
日期:2024-05-23
卷期号:165 (7)
被引量:1
标识
DOI:10.1210/endocr/bqae059
摘要
Abstract Leukocyte cell-derived chemotaxin 2 (LECT2) is a protein initially isolated as a neutrophil chemotactic factor. We previously found that LECT2 is an obesity-associated hepatokine that senses liver fat and induces skeletal muscle insulin resistance. In addition, hepatocyte-derived LECT2 activates macrophage proinflammatory activity by reinforcing the lipopolysaccharide (LPS)-induced c-Jun N-terminal kinase signaling. Based on these findings, we examined the effect of LECT2 deletion on nonalcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) caused by bacterial translocation. We created the bacterial translocation-mediated NAFLD/NASH model using LECT2 knockout mice (LECT2 KO) with 28 times a low-dose LPS injection under high-fat diet feeding conditions. LECT2 deletion exacerbated steatosis and significantly reduced p38 phosphorylation in the liver. In addition, LECT2 deletion increased macrophage infiltration with decreased M1/M2 ratios. LECT2 might contribute to protecting against lipid accumulation and macrophage activation in the liver under pathological conditions, which might be accomplished via p38 phosphorylation. This study provides novel aspects of LECT2 in the bacterial translocation-mediated NAFLD/NASH model.
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