Department of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine Graduate School of Medical Science; Kyoto, Japan.
Islets. 2010 Jul-Aug;2(4):258-60. doi: 10.4161/isl.2.4.12157.
In our recent paper, we proposed that senescence marker protein-30 (SMP30) could be a novel molecule which was involved in an impairment of β-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 β-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.
在我们最近的一篇论文中，我们提出衰老标志物蛋白-30（SMP30）可能是一种新的分子，它参与了衰老过程中β细胞功能的损伤。SMP30 敲除（KO）小鼠和野生型（WT）小鼠从 7 周龄开始分别用标准饮食（SD）或高脂肪饮食（HFD）喂养 8 周。在 15 周龄时进行的腹腔内葡萄糖耐量试验中，与 SD 喂养的 WT 小鼠相比，SD 喂养的 KO 小鼠在葡萄糖给药后 30 分钟时的血糖水平显著升高了 25%。与 SD 喂养的 WT 小鼠相比，SD 喂养的 KO 小鼠在葡萄糖后 30 分钟时的胰岛素水平显著降低了 37%。有趣的是，胰岛素耐量试验显示 SD 喂养的 KO 小鼠的降血糖作用更大。形态计量学分析显示，β细胞质量和增殖的 HFD 诱导代偿性增加程度没有差异。综上所述，这些数据表明 KO 小鼠的葡萄糖耐量受损是由于胰岛素分泌早期阶段受损所致。SMP30 的减少可能导致正常衰老过程中葡萄糖耐量的恶化。
