A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice.
A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice.
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代谢综合征的小鼠模型；内脏脂肪组织的增加先于高脂饮食喂养的雄性KK/TA小鼠的脂肪肝和胰岛素抵抗的发展。
DOI：
10.3164/jcbn.2008022
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发表时间：
2008-03
影响因子：
2.4
通讯作者：
Yoshikawa, Toshikazu
中科院分区：
文献类型：
--
作者：
Akagiri, Satomi;Naito, Yuji;Ichikawa, Hiroshi;Mizushima, Katsura;Takagi, Tomohisa;Handa, Osamu;Kokura, Satoshi;Yoshikawa, Toshikazu
为了确定肥胖和内脏白色脂肪组织(WAT)对代谢综合征的相对贡献，我们利用雄性KK/Ta小鼠建立了一个易受高脂饮食诱导的肥胖和胰岛素抵抗影响的模型。在10周龄、14周龄和22周龄的小鼠中，高脂饮食组的Wat体重与体重的比率比对照组大。内脏WAT的增加先于脂肪肝和胰岛素抵抗的发展。在血浆脂联素水平下降或发生胰岛素抵抗之前，WAT中脂联素mRNA的表达明显降低。22周龄小鼠肝脏脂肪浸润和肿瘤坏死因子-α表达与胰岛素抵抗有关。这些数据表明，我们的小鼠模型将有助于未来研究内脏水及其产物在代谢综合征发展中的作用。
To determine the relative contribution of obesity and visceral white adipose tissue (WAT) to metabolic syndrome, we developed a model that is susceptible to high-fat diet-induced obesity and insulin resistance using male KK/Ta mice. The ratio of WAT weight to body weight was greater in the high-fat diet group compared with the control group in 10-, 14-, and 22-week-old mice. The increase in visceral WAT preceded development of fatty liver and insulin resistance. Adiponectin mRNA expression in WAT was markedly decreased before the decrease in its plasma levels or the development of insulin resistance. Insulin resistance appeared in association with fatty infiltration and TNF-α expression in the liver in 22-week-old mice. These data indicate that our mouse model would be useful for future studies that investigate the role of visceral WAT and its products in the development of metabolic syndrome.
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DOI：
10.1152/ajpendo.00171.2007
发表时间：
2007-08-01
影响因子：
5.1
作者：
Coenen, Kimberly R.;Hasty, Alyssa H.
通讯作者：
Hasty, Alyssa H.
影响因子：
82.9
作者：
Yamauchi, T;Kamon, J;Kadowaki, T
通讯作者：
Kadowaki, T
影响因子：
4.8
作者：
Lee, JY;Sohn, KH;Hwang, D
通讯作者：
Hwang, D
影响因子：
4.8
作者：
Hu, E;Liang, P;Spiegelman, BM
通讯作者：
Spiegelman, BM
影响因子：
9.8
作者：
Onat, A;Hergenç, G;Sansoy, V
通讯作者：
Sansoy, V