Involvement of stanniocalcins in the deregulation of glycaemia in obese mice and type 2 diabetic patients.
Involvement of stanniocalcins in the deregulation of glycaemia in obese mice and type 2 diabetic patients.
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DOI：
10.1111/jcmm.13355
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发表时间：
2018-01
影响因子：
5.3
通讯作者：
Redondo PC
中科院分区：
文献类型：
--
作者：
López JJ;Jardín I;Cantonero Chamorro C;Duran ML;Tarancón Rubio MJ;Reyes Panadero M;Jiménez F;Montero R;González MJ;Martínez M;Hernández MJ;Brull JM;Corbacho AJ;Delgado E;Granados MP;Gómez-Gordo L;Rosado JA;Redondo PC
斯钙素在胰腺组织中表达，并且表明人中循环胰岛素和STC 2浓度之间直接相关。在这里，我们显示了一个显着的相关性之间的STC 1和糖尿病2患者的血糖和糖化血红蛋白，而DM 2患者谁目前最大的糖化血红蛋白值表现出最低的STC 2表达。然而，用抗血小板药物治疗患者不会显著改变两种STC的表达。另一方面，表现出新生儿和成年超重的STC 2 <$/<$小鼠在喂食高热量饮食（繁殖颗粒，BP）时进一步表现出失调性贫血。这种变化在动物生命的早期阶段更为明显。使用葡萄糖口服试验证实这些小鼠中的失调性高血糖症。此外，STC 2-/-小鼠的胰腺大小增加;因此，组织学分析表明，WT小鼠通过诱导细胞分裂增加胰岛大小来响应BP饮食，而STC 2-/-小鼠缺乏这种代偿机制。相反，BP喂养的STC 2-/-小鼠显示出增加的胰岛数量，但与用常规颗粒喂养的小鼠相比具有相似的大小。组织学分析表明，STC 2-/-小鼠的组织结构破坏和红细胞浸润，可能是由于BP饮食引起的应激。最后，在STC 2-/-小鼠的胰岛中观察到胰高血糖素免疫染色增强，胰高血糖素ELISA测定证实循环胰高血糖素增加。总之，我们提出的证据表明，STCs的作用，主要是STC 2，作为一个可能的早期标志物在糖尿病的发展。
Stanniocalcins are expressed in the pancreas tissue, and it was suggested a direct correlation between circulating insulin and STC2 concentrations in human. Here, we show a significant correlation between STC1 and both glycaemia and glycosylated haemoglobin among DM2 patients, while DM2 patients who present the greatest glycosylated haemoglobin values exhibited the lowest STC2 expression. However, treatment of patients with antiglycaemic drugs does not significantly modify the expression of both STCs. On the other hand, STC2‐/‐ mice that exhibited neonatal and adult overweight further presented deregulated glycaemia when they were feed with a hypercaloric diet (breeding pellet, BP). This alteration is more evident at the early stages of the animal life. Deregulated glycaemia in these mice was confirmed using glucose oral test. In addition, STC2‐/‐ mice present enhanced pancreas size; thus, the histological analysis reveals that WT mice respond to BP diet by increasing the size of the pancreatic islets through inducing cell division, and STC2‐/‐ mice lack this compensatory mechanism. Contrary, BP fed STC2‐/‐ mice show enhanced number of islets but of similar size than those fed with regular pellet. Histopathological analysis demonstrates tissue structure disruption and erythrocytes infiltrations in STC2‐/‐ mice, possibly due to the stress evoked by the BP diet. Finally, enhanced glucagon immunostaining was observed in the islet of STC2‐/‐ mice, and the glucagon ELISA assay confirmed the increase in the circulating glucagon. Summarizing, we present evidence of the role of STCs, mainly STC2, as a possible early marker during development of diabetes mellitus.
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DOI：
10.1016/s0140-6736(14)60613-9
发表时间：
2014-06-07
期刊：
Lancet (London, England)
影响因子：
--
作者：
Ley SH;Hamdy O;Mohan V;Hu FB
通讯作者：
Hu FB
影响因子：
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作者：
Fazio EN;Dimattia GE;Chadi SA;Kernohan KD;Pin CL
通讯作者：
Pin CL
影响因子：
1.9
作者：
Piccini, Barbara;Artuso, Rosangela;Toni, Sonia
通讯作者：
Toni, Sonia
影响因子：
19.6
作者：
通讯作者：
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DOI：
10.1016/j.bbapap.2014.11.002
发表时间：
2015-06-01
影响因子：
3.2
作者：
Na, Sang-su;Aldonza, Mark Borris;Cho, Je-Yoel
通讯作者：
Cho, Je-Yoel