首页> 外文期刊>Journal of clinical biochemistry and nutrition. >Lemon Polyphenols Suppress Diet-induced Obesity by Up-Regulation of mRNA Levels of the Enzymes Involved in beta-Oxidation in Mouse White Adipose Tissue
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Lemon Polyphenols Suppress Diet-induced Obesity by Up-Regulation of mRNA Levels of the Enzymes Involved in beta-Oxidation in Mouse White Adipose Tissue

机译:柠檬多酚通过上调小鼠白脂肪组织中β-氧化酶mRNA的水平来抑制饮食诱导的肥胖。

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The aim of this study was to investigate the effect of dietary lemon polyphenols on high-fat diet-induced obesity in mice, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. Mice were divided into three groups and fed either a low fat diet (LF) or a high fat diet (HF) or a high fat diet supplemented with 0.5% w/w lemon polyphenols (LP) extracted from lemon peel for 12 weeks. Body weight gain, fat pad accumulation, the development of hyperlipidemia, hyperglycemia, and insulin resistance were significantly suppressed by lemon polyphenols. Supplementation with lemon polyphenols also significantly up-regulated the mRNA level of the peroxisome proliferator activated receptor-alpha (PPAR alpha) compared to the LF and HF groups in the liver. Furthermore, the mRNA level of acyl-CoA oxidase (ACO) was up-regulated in the LP group compared to the LF group, but not HF group in the liver, and was also significantly increased in the epididymal white adipose tissue. Thus, feeding with lemon polyphenols suppressed body weight gain and body fat accumulation by increasing peroxisomal beta-oxidation through up-regulation of the mRNA level of ACO in the liver and white adipose tissue, which was likely mediated via up-regulation of the mRNA levels of PPAR alpha.
机译:这项研究的目的是研究饮食中柠檬多酚对高脂饮食诱导的肥胖症小鼠的影响,以及对参与脂质代谢的基因表达的调控以阐明其机制。将小鼠分为三组,并喂养低脂饮食(LF)或高脂饮食(HF)或高脂饮食,并补充从柠檬皮中提取的0.5%w / w柠檬多酚(LP),持续12周。柠檬多酚可显着抑制体重增加,脂肪垫堆积,高脂血症,高血糖症和胰岛素抵抗的发生。与肝脏中的LF和HF组相比,补充柠檬多酚还显着上调了过氧化物酶体增殖物激活的受体α(PPAR alpha)的mRNA水平。此外,与LF组相比,LP组中的酰基辅酶A氧化酶(ACO)的mRNA水平在肝脏中被上调,而在HF组中则没有,在附睾的白色脂肪组织中也显着增加。因此,饲喂柠檬多酚可通过上调肝脏和白色脂肪组织中ACO的mRNA水平来增加过氧化物酶体β-氧化作用,从而抑制体重增加和体内脂肪积累,这很可能是通过上调mRNA水平来介导的PPAR alpha。

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