高思源, 袁小玲, 孙星, 王婷, 陈一辰, 傅继华. 高脂饲料喂养结合慢性应激:一种新颖的大鼠代谢综合征模型的特点[J]. 环境与职业医学, 2012, 29(8): 501-505.
引用本文: 高思源, 袁小玲, 孙星, 王婷, 陈一辰, 傅继华. 高脂饲料喂养结合慢性应激:一种新颖的大鼠代谢综合征模型的特点[J]. 环境与职业医学, 2012, 29(8): 501-505.
GAO Si-yuan , YUAN Xiao-ling , SUN Xing , WANG Ting , CHEN Yi-chen , FU Ji-hua . Combination of High Fat Diet and Chronic Stress: Characteristics of a Novel Metabolic Syndrome Rat Model[J]. Journal of Environmental and Occupational Medicine, 2012, 29(8): 501-505.
Citation: GAO Si-yuan , YUAN Xiao-ling , SUN Xing , WANG Ting , CHEN Yi-chen , FU Ji-hua . Combination of High Fat Diet and Chronic Stress: Characteristics of a Novel Metabolic Syndrome Rat Model[J]. Journal of Environmental and Occupational Medicine, 2012, 29(8): 501-505.

高脂饲料喂养结合慢性应激:一种新颖的大鼠代谢综合征模型的特点

Combination of High Fat Diet and Chronic Stress: Characteristics of a Novel Metabolic Syndrome Rat Model

  • 摘要: 目的 研究高脂饲料(high fat diet,HFD)结合慢性应激(chronic stress,CS)致大鼠代谢综合征模型的特点。

    方法 将32 只雄性Wistar 大鼠随机分为对照组、HFD喂养组、CS 刺激组及HFD喂养结合CS 刺激(HFD+CS)组,每组8 只。持续处理12 周后,检测胰岛素抵抗、血酯及血皮质醇水平,肝脏总胆固醇、三酰甘油总含量及水溶性成分含量,肝脏氧化应激、炎症程度及肝X受体α(liver X receptor α,LXRα)、过氧化物酶体增生物激活受体γ(peroxisome proliferator-activated receptor γ,PPARγ)基因表达,内脏脂肪含量及其内分泌功能。

    结果 慢性应激可恶化由高脂饲料引起的胰岛素抵抗、血脂紊乱、肝脏氧化应激、炎症及脂肪组织内分泌紊乱。该代谢综合征模型的明显特点是肝脏水溶性总胆固醇、三酰甘油含量明显升高,肝脏LXRα、PPARγ mRNA表达进一步下调,血皮质醇浓度升高。

    结论 高脂饲料结合慢性应激可建立具有典型代谢综合征特征的大鼠模型,慢性应激可恶化高脂饲料引起的代谢综合征病变。

     

    Abstract: Objective To observe the characteristics of a metabolic syndrome (MS) model induced by the combination of high fat diet (HFD) and chronic stress (CS) in rats.

    Methods Thirty-two male Wistar rats were randomly divided into 4 groups: fed on either a standard chow diet or a HFD and given chronic stress or not for 12 weeks. Insulin resistance (IR), levels of serum cortisol, levels of hepatic total cholesterol (TC) and triglyceride (TG) and their water-soluble components, hepatic oxidative stress and inflammation in liver, mRNA expressions of liver X receptor α (LXRα) and peroxisome proliferator-activated receptor γ (PPARγ) in liver, and visceral fat and endocrine function were detected and evaluated.

    Results CS could aggravate IR, dyslipidemia, hepatic inflammation and oxidative stress, and adipose tissue endocrine disorders in rats. The characteristics of this model were further elevated hepatic water-soluble components of TC and TG (deleterious lipoprotein), further down-regulated mRNA expressions of LXRα and PPARγ, and increased levels of serum cortisol.

    Conclusion The combination of HFD and CS in male Wistar rats could induce a typical MS model, and CS can aggravate MS status induced by HFD.

     

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