胰岛素抵抗和糖尿病仓鼠（金黄地鼠）的胰岛素抵抗与参与脂质和葡萄糖代谢的基因的肝脏异常表达有关。
Insulin resistance in insulin-resistant and diabetic hamsters (Mesocricetus auratus) is associated with abnormal hepatic expression of genes involved in lipid and glucose metabolism.
作者信息
Li Guosheng, Liu Xuhan, Zhu Hua, Huang Lan, Liu Yali, Ma Chunmei, Qin Chuan
机构信息
Department of Pathology, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) and Peking Union Medical College (PUMC), Beijing, China.
出版信息
Comp Med. 2009 Oct;59(5):449-58.
Fat-induced hepatic insulin resistance (FIHIR) in obesity induced by high-fat diet leads to ectopic lipid accumulation and may contribute to the pathogenesis of type 2 diabetes. We examined the alterations in hepatic gene expression involved in FIHIR by using obese insulin-resistant and diabetic hamsters that received high-fat diet with or without low-dose streptozotocin. Microarray analysis and confirmatory real-time RT-PCR indicated that increased mRNA levels of sterol regulatory element-binding proteins (SREBPs) and decreased mRNA levels of liver X receptor (LXRalpha) and peroxisome-proliferator-activated receptor (PPARalpha) occurred in FIHIR in insulin-resistant and diabetic hamsters. Expression levels of hepatic LXRalpha, SREBPs, and PPARalpha differed significantly between insulin-resistant and diabetic hamsters. Expression of LXRalpha, SREBPs, and PPARalpha all change in FIHIR associated with hepatic lipid accumulation in insulin-resistant and diabetic hamsters in which disease is induced by high-fat diet and streptozotocin injection.
高脂饮食诱导的肥胖中的脂肪诱导性肝胰岛素抵抗（FIHIR）会导致异位脂质蓄积，并可能促成2型糖尿病的发病机制。我们通过使用接受高脂饮食且伴有或不伴有低剂量链脲佐菌素的肥胖胰岛素抵抗和糖尿病仓鼠，研究了与FIHIR相关的肝脏基因表达变化。微阵列分析和验证性实时逆转录聚合酶链反应表明，在胰岛素抵抗和糖尿病仓鼠的FIHIR中，固醇调节元件结合蛋白（SREBPs）的mRNA水平升高，而肝脏X受体（LXRα）和过氧化物酶体增殖物激活受体（PPARα）的mRNA水平降低。胰岛素抵抗和糖尿病仓鼠之间肝脏LXRα、SREBPs和PPARα的表达水平存在显著差异。在由高脂饮食和链脲佐菌素注射诱导疾病的胰岛素抵抗和糖尿病仓鼠中，LXRα、SREBPs和PPARα的表达在与肝脏脂质蓄积相关的FIHIR中均发生变化。
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