Decreased senescence marker protein-30 could be a factor that contributes to the worsening of glucose tolerance in normal aging
Decreased senescence marker protein-30 could be a factor that contributes to the worsening of glucose tolerance in normal aging
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DOI：
10.4161/isl.2.4.12157
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发表时间：
2010-07-01
期刊：
影响因子：
2.2
通讯作者：
Hasegawa, Goji
中科院分区：
文献类型：
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作者：
Hasegawa, Goji
在我们最近的论文中，我们提出衰老标记蛋白-30(SMP30)可能是一个新的分子，它参与了随着年龄的增长而导致的胰岛细胞功能的损害。SMP30基因敲除(KO)小鼠和野生型(WT)小鼠从7周龄开始分别饲喂标准饲料(SD)和高脂饲料(HFD)8周。在15周龄的腹膜糖耐量试验中，饲喂SD的KO小鼠的血糖水平在给药后30分钟显著高于饲喂SD的WT小鼠25%。与SD喂养的WT小鼠相比，在葡萄糖后30分钟，SD喂养的KO小鼠的胰岛素水平显著降低37%。有趣的是，胰岛素耐量测试显示，SD喂养的KO小鼠有更大的降糖效果。形态计量学分析表明，HFD诱导的β细胞质量和增殖的代偿性增加程度没有差异。总而言之，这些数据表明，胰岛素分泌早期的损害是导致KO小鼠葡萄糖不耐受的原因。SMP30降低可能是正常衰老时糖耐量恶化的原因之一。
In our recent paper, we proposed that senescence marker protein-30 (SMP30) could be a novel molecule which was involved in an impairment of beta-cell function with aging. SMP30 knockout (KO) mice and wild-type (WT) mice were fed a standard diet (SD) or a high fat diet (HFD) for 8 weeks from 7 weeks of age. In an intraperitoneal glucose tolerance test at 15 weeks of age, blood glucose levels in SD-fed KO mice were significantly increased by 25% at 30 min after glucose administration compared to SD-fed WT mice. Insulin levels in SD-fed KO mice were significantly decreased by 37% at 30 min postglucose compared to SD-fed WT mice. Interestingly, an insulin tolerance test showed a greater glucose lowering effect in SD-fed KO mice. Morphometric analysis revealed no differences in the degree of HFD-induced compensatory increase in beta-cell mass and proliferation. Collectively, these data indicate that impairment of the early phase of insulin secretion underlies glucose intolerance in KO mice. Decreased SMP30 may contribute to the worsening of glucose tolerance that occurs in normal aging.