Loss of mPer2 increases plasma insulin levels by enhanced glucose‐stimulated insulin secretion and impaired insulin clearance in mice
Loss of mPer2 increases plasma insulin levels by enhanced glucose‐stimulated insulin secretion and impaired insulin clearance in mice
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DOI：
10.1016/j.febslet.2012.03.034
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发表时间：
2012-05
期刊：
影响因子：
3.5
通讯作者：
Yue Zhao;Ying Zhang;Mengyi Zhou;Shiming Wang;Z. Hua;Jianfa Zhang
中科院分区：
文献类型：
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作者：
Yue Zhao;Ying Zhang;Mengyi Zhou;Shiming Wang;Z. Hua;Jianfa Zhang
外周振荡的存在已被证明，它们对组织整个身体的代谢至关重要。在这里，我们发现与野生型小鼠相比，缺乏mPer2的小鼠明显增加了循环胰岛素水平。葡萄糖更有效地刺激胰岛素分泌，葡萄糖类似物四氧嘧啶在mper2缺陷小鼠中诱导更严重的高血糖。肝脏胰岛素降解酶（Ide）表现出明显的昼夜节律，在mper2缺陷小鼠中，这种节律受损，导致胰岛素清除率降低。mPer2缺失导致Clock表达增加，Mkp1和Ide1表达减少，这可能是观察到的表型的基础，并表明mPer2在调节循环胰岛素水平中起作用。
The existence of peripheral oscillators has been shown, and they are critically important for organizing the metabolism of the whole body. Here we show that mice deficient in mPer2 markedly increase circulatory levels of insulin compared with wild type mice. Insulin secretion was more effectively stimulated by glucose, and alloxan, a glucose analogue, induced more severe hyperglycemia in mPer2-deficient mice. Hepatic insulin degrading enzyme (Ide) displayed an obvious day and night rhythm, which was impaired in mPer2-deficient mice, leading to a decrease in insulin clearance. Deficiency in mPer2 caused increased Clock expression and decreased expression of Mkp1 and Ide1, possibly underlying the observed phenotypes and suggesting that mPer2 plays a role in regulation of circulating insulin levels.