β氧化
辅酶A
过氧化物酶体
脂肪酸
生物化学
肉碱
脂肪变性
化学
脂肪酸合酶
线粒体
脂肪酸合成
乙酰辅酶A羧化酶
脂肪肝
生物
酶
内分泌学
内科学
丙酮酸羧化酶
还原酶
医学
基因
疾病
作者
Jiarui Zhang,Sainan Wang,Junyao Wang,Wenhao Liu,Hao Gong,Zhao Zhang,Bo Lyu,Hansong Yu
出处
期刊:Foods
[MDPI AG]
日期:2023-05-22
卷期号:12 (10): 2081-2081
被引量:1
标识
DOI:10.3390/foods12102081
摘要
Numerous investigations have shown that insoluble dietary fiber (IDF) has a potentially positive effect on obesity due to a high-fat diet (HFD). Our previous findings based on proteomic data revealed that high-purity IDF from soybean residue (okara) (HPSIDF) prevented obesity by regulating hepatic fatty acid synthesis and degradation pathways, while its intervention mechanism is uncharted. Consequently, the goal of this work is to find out the potential regulatory mechanisms of HPSIDF on hepatic fatty acid oxidation by determining changes in fatty acid oxidation-related enzymes in mitochondria and peroxisomes, the production of oxidation intermediates and final products, the composition and content of fatty acids, and the expression levels of fatty acid oxidation-related proteins in mice fed with HFD. We found that supplementation with HPSIDF significantly ameliorated body weight gain, fat accumulation, dyslipidemia, and hepatic steatosis caused by HFD. Importantly, HPSIDF intervention promotes medium- and long-chain fatty acid oxidation in hepatic mitochondria by improving the contents of acyl-coenzyme A oxidase 1 (ACOX1), malonyl coenzyme A (Malonyl CoA), acetyl coenzyme A synthase (ACS), acetyl coenzyme A carboxylase (ACC), and carnitine palmitoyl transferase-1 (CPT-1). Moreover, HPSIDF effectively regulated the expression levels of proteins involved with hepatic fatty acid β-oxidation. Our study indicated that HPSIDF treatment prevents obesity by promoting hepatic mitochondrial fatty acid oxidation.
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