CTRP2 overexpression improves insulin and lipid tolerance in diet-induced obese mice.
CTRP2 overexpression improves insulin and lipid tolerance in diet-induced obese mice.
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DOI：
10.1371/journal.pone.0088535
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Wong GW
中科院分区：
文献类型：
--
作者：
Peterson JM;Seldin MM;Tan SY;Wong GW
CTRP 2是C1q家族的分泌型血浆蛋白，其增强培养的肌管中的糖原沉积和脂肪氧化。然而，其体内代谢功能尚未确定。我们在这里表明，急性和慢性代谢紊乱引起的禁食或高脂肪喂养上调Ctrp 2的mRNA表达在白色脂肪组织，而不影响其循环血浆水平。我们建立了一个转基因小鼠模型，CTRP 2的循环水平升高，以确定其在体内的代谢功能。当喂食低脂饮食时，野生型和CTRP 2转基因小鼠没有表现出代谢表型。当用高脂饮食诱导肥胖时，野生型和CTRP 2转基因小鼠具有相似的体重增加、肥胖、食物摄入、代谢率和能量消耗。两组小鼠的空腹血脂和脂肪因子谱也相似。然而，虽然野生型和CTRP 2转基因小鼠在禁食状态下的葡萄糖和胰岛素水平相当，但转基因小鼠在进食状态下的胰岛素水平始终较低。值得注意的是，相对于同窝对照，CTRP 2转基因小鼠具有改善的胰岛素耐受性和更大的处理急性脂质挑战的能力。我们的研究结果首次强调了CTRP 2在调节全身代谢中的体内作用。
CTRP2 is a secreted plasma protein of the C1q family that enhances glycogen deposition and fat oxidation in cultured myotubes. Its in vivo metabolic function, however, has not been established. We show here that acute and chronic metabolic perturbations induced by fasting or high-fat feeding up-regulated the mRNA expression of Ctrp2 in white adipose tissue without affecting its circulating plasma levels. We generated a transgenic mouse model with elevated circulating levels of CTRP2 to determine its metabolic function in vivo. When fed a low-fat diet, wild-type and CTRP2 transgenic mice exhibited no metabolic phenotypes. When challenged with a high-fat diet to induce obesity, wild-type and CTRP2 transgenic mice had similar weight gain, adiposity, food intake, metabolic rate, and energy expenditure. Fasting serum lipid and adipokine profiles were also similar between the two groups of mice. However, while glucose and insulin levels in the fasted state were comparable between wild-type and CTRP2 transgenic mice, insulin levels in the fed state were consistently lower in transgenic mice. Notably, CTRP2 transgenic mice had improved insulin tolerance and a greater capacity to handle acute lipid challenge relative to littermate controls. Our results highlight, for the first time, the in vivo role of CTRP2 in modulating whole-body metabolism.
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影响因子：
4.8
作者：
Wei, Zhikui;Peterson, Jonathan M.;Wong, G. William
通讯作者：
Wong, G. William
DOI：
10.1073/pnas.0403760101
发表时间：
2004-07-13
影响因子：
11.1
作者：
Wong, GW;Wang, J;Lodish, HF
通讯作者：
Lodish, HF
影响因子：
9.5
作者：
Su H;Yuan Y;Wang XM;Lau WB;Wang Y;Wang X;Gao E;Koch WJ;Ma XL
通讯作者：
Ma XL
影响因子：
4.8
作者：
Seldin, Marcus M.;Peterson, Jonathan M.;Wong, G. William
通讯作者：
Wong, G. William
DOI：
10.1161/atvbaha.111.231050
发表时间：
2011-11
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Zheng Q;Yuan Y;Yi W;Lau WB;Wang Y;Wang X;Sun Y;Lopez BL;Christopher TA;Peterson JM;Wong GW;Yu S;Yi D;Ma XL
通讯作者：
Ma XL