脂肪肝
脂肪变性
内科学
氧化应激
内分泌学
医学
脂联素
CD36
生物
肥胖
疾病
胰岛素抵抗
受体
作者
Guillermo Santos‐Sánchez,Iván Cruz-Chamorro,Ana Isabel Álvarez‐Ríos,José M. Fernández‐Santos,Victoria Vázquez‐Román,Beatriz Rodríguez-Ortiz,Nuria Álvarez‐Sánchez,Ana Isabel Álvarez‐López,María C. Millán-Linares,Francisco Millán,Justo Pedroche,María‐Soledad Fernández‐Pachón,Patricia Judith Lardone,Juan Miguel Guerrero,Ignacio Bejarano,Antonio Carrillo‐Vico
出处
期刊:Antioxidants
[MDPI AG]
日期:2021-07-29
卷期号:10 (8): 1222-1222
被引量:19
标识
DOI:10.3390/antiox10081222
摘要
Metabolic-associated fatty liver disease (MAFLD) is the most important cause of liver disease worldwide. It is characterized by the accumulation of fat in the liver and is closely associated with abdominal obesity. In addition, oxidative stress and inflammation are significant features involved in MAFLD. Recently, our group demonstrated that lupin protein hydrolysates (LPHs) had lipid lowering, antioxidant, and anti-inflammatory effects. Sixty male mice fed with a Western diet were intragastrically treated with LPHs (or vehicle) for 12 weeks. Liver and adipose tissue lipid accumulation and hepatic inflammatory and oxidant status were evaluated. A significant decrease in steatosis was observed in LPHs-treated mice, which presented a decreased gene expression of CD36 and LDL-R, crucial markers in MAFLD. In addition, LPHs increased the hepatic total antioxidant capacity and reduced the hepatic inflammatory status. Moreover, LPHs-treated mice showed a significant reduction in abdominal adiposity. This is the first study to show that the supplementation with LPHs markedly ameliorates the generation of the steatotic liver caused by the intake of a Western diet and reduces abdominal obesity in ApoE−/− mice. Future clinical trials should shed light on the effects of LPHs on MAFLD.
科研通智能强力驱动
Strongly Powered by AbleSci AI