Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling.
Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling.
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DOI：
10.1038/ncomms1905
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发表时间：
2012-06-12
影响因子：
16.6
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中科院分区：
文献类型：
--
作者：
胰岛素和胰岛素样生长因子1（IGF-1）在脂肪细胞分化、糖耐量和胰岛素敏感性中起重要作用。在这里，为了评估这些途径如何相互补偿，我们创建了对胰岛素和IGF-1受体进行双重组织特异性敲除的小鼠，以消除脂肪中的所有胰岛素/IGF-1信号传导。这些FIGIRKO小鼠具有显著减少的白色和棕色脂肪量，并且完全抵抗高脂饮食（HFD）诱导的肥胖和年龄和HFD诱导的葡萄糖耐受不良。FIGIRKO小鼠的能量消耗增加，尽管棕色脂肪量减少>85%。然而，FIGIRKO小鼠在置于4°C时不能保持体温。FIGIRKO小鼠的棕色脂肪活性显著降低，但对β3受体刺激有反应。因此，胰岛素/IGF-1信号传导在控制棕色和白色脂肪发育中具有关键作用，并且当被破坏时，导致产热缺陷和基础代谢率的矛盾增加。
Insulin and insulin-like growth factor 1 (IGF-1) play important roles in adipocyte differentiation, glucose tolerance and insulin sensitivity. Here, to assess how these pathways can compensate for each other, we created mice with a double tissue-specific knockout of insulin and IGF-1 receptors to eliminate all insulin/IGF-1 signaling in fat. These FIGIRKO mice had markedly decreased white and brown fat mass and were completely resistant to high fat diet (HFD) induced obesity and age- and HFD-induced glucose intolerance. Energy expenditure was increased in FIGIRKO mice despite a >85% reduction in brown fat mass. However, FIGIRKO mice were unable to maintain body temperature when placed at 4°C. Brown fat activity was markedly decreased in FIGIRKO mice but was responsive to β3-receptor stimulation. Thus, insulin/IGF-1 signaling has a crucial role in the control of brown and white fat development, and, when disrupted, leads to defective thermogenesis and a paradoxical increase in basal metabolic rate.
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影响因子：
7.7
作者：
Saito M;Okamatsu-Ogura Y;Matsushita M;Watanabe K;Yoneshiro T;Nio-Kobayashi J;Iwanaga T;Miyagawa M;Kameya T;Nakada K;Kawai Y;Tsujisaki M
通讯作者：
Tsujisaki M
影响因子：
4.8
作者：
Golozoubova, V;Hohtola, E;Nedergaard, J
通讯作者：
Nedergaard, J
影响因子：
64.8
作者：
Enerback, S;Jacobsson, A;Kozak, LP
通讯作者：
Kozak, LP
影响因子：
7.3
作者：
Boucher J;Macotela Y;Bezy O;Mori MA;Kriauciunas K;Kahn CR
通讯作者：
Kahn CR
影响因子：
4.8
作者：
Entingh-Pearsall, A;Kahn, CR
通讯作者：
Kahn, CR