脂联素通过 AMPK 信号通路调节脂质积累和炎症反应，从而促进非酒精性脂肪性肝病的发生。

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a primary contributor to liver-related morbidity and mortality. Asprosin has been reported to be implicated in NAFLD. AIMS: This work is to illuminate the effects of Asprosin on NAFLD and the possible downstream mechanism. MATERIALS & METHODS: The weight of NAFLD mice induced by a high-fat diet was detected. Quantitative reverse-transcription polymerase chain reaction (RT-qPCR) examined serum Asprosin expression. RT-qPCR and western blot analysis examined Asprosin expression in mice liver tissues. Intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were implemented. Biochemical kits tested liver enzyme levels in mice serum and liver tissues. Hematoxylin and eosin staining evaluated liver histology. Liver weight was also tested and oil red O staining estimated lipid accumulation. RT-qPCR and western blot analysis analyzed the expression of gluconeogenesis-, fatty acid biosynthesis-, fatty acid oxidation-, and inflammation-associated factors. Besides, western blot analysis examined the expression of AMP-activated protein kinase (AMPK)/p38 signaling-associated factors. In palmitic acid (PA)-treated mice hepatocytes, RT-qPCR and western blot analysis examined Asprosin expression. Lipid accumulation, gluconeogenesis, fatty acid biosynthesis, fatty acid oxidation, and inflammation were appraised again. RESULTS: Asprosin was overexpressed in the serum and liver tissues of NAFLD mice and PA-treated mice hepatocytes. Asprosin interference reduced mice body and liver weight, improved glucose tolerance and diminished liver injury in vivo. Asprosin knockdown alleviated lipid accumulation and inflammatory infiltration both in vitro and in vivo. Additionally, Asprosin absence activated AMPK/p38 signaling and AMPK inhibitor Compound C reversed the impacts of Asprosin on lipid accumulation and inflammatory response. CONCLUSION: Collectively, Asprosin inhibition suppressed lipid accumulation and inflammation to obstruct NAFLD through AMPK/p38 signaling.

背景：非酒精性脂肪性肝病（NAFLD）是导致与肝脏相关的发病率和死亡率的主要原因。有报道称，天门冬素与 NAFLD 有关。

目的：本研究旨在阐明天门冬素对 NAFLD 的影响及其可能的下游机制。

材料与方法：检测高脂肪饮食诱导的 NAFLD 小鼠的体重。定量逆转录聚合酶链反应（RT-qPCR）检测血清天门冬素表达。RT-qPCR 和 Western blot 分析检测小鼠肝组织中天冬素的表达。进行腹腔内葡萄糖耐量试验（IPGTT）和腹腔内胰岛素耐量试验（IPITT）。生化试剂盒检测小鼠血清和肝组织中的肝酶水平。苏木精和伊红染色评估肝组织学。还检测了肝重和油红 O 染色评估脂质积累。RT-qPCR 和 Western blot 分析检测糖异生、脂肪酸合成、脂肪酸氧化和炎症相关因子的表达。此外，Western blot 分析检测 AMP 激活的蛋白激酶（AMPK）/p38 信号相关因子的表达。在棕榈酸（PA）处理的小鼠肝细胞中，进行 RT-qPCR 和 Western blot 分析检测天门冬素的表达。再次评估脂质积累、糖异生、脂肪酸合成、脂肪酸氧化和炎症。

结果：天门冬素在 NAFLD 小鼠和 PA 处理的小鼠肝细胞的血清和肝组织中过度表达。天冬素干扰减少了小鼠的体重和肝重，改善了体内葡萄糖耐量并减轻了肝损伤。天冬素敲低减轻了体外和体内的脂质积累和炎症浸润。此外，天冬素缺乏激活了 AMPK/p38 信号，而 AMPK 抑制剂 Compound C 逆转了天冬素对脂质积累和炎症反应的影响。

结论：总之，天冬素抑制通过 AMPK/p38 信号抑制脂质积累和炎症反应，从而阻止 NAFLD 的发生。