Channeling dysglycemia: ion-channel variations perturbing glucose homeostasis.
Channeling dysglycemia: ion-channel variations perturbing glucose homeostasis.
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DOI：
10.1016/j.tem.2011.09.004
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发表时间：
2012-01
影响因子：
10.9
通讯作者：
Jacobson, David Aaron
中科院分区：
文献类型：
--
作者：
Denton, Jerod Scott;Jacobson, David Aaron
维持血糖稳态是一个依赖于胰岛激素分泌的复杂过程。胰岛的激素分泌与钙离子进入有关，钙离子进入是再生胰岛细胞电活动的结果。因此，调节钙进入胰岛细胞的离子机制对维持正常的葡萄糖稳态至关重要。全基因组关联研究已经确定了单核苷酸多态性，包括位于离子通道或相关亚基基因中或附近的五个，其显示与以代谢障碍为特征的人类疾病相关。本文综述了与人体葡萄糖稳态紊乱相关的离子通道基因的多态性和突变，并讨论了它们在调节胰岛激素分泌中的潜在作用。
Maintaining blood glucose homeostasis is a complex process dependent on pancreatic islet hormone secretion. Hormone secretion from islets is coupled to calcium entry, which results from regenerative islet cell electrical activity. Therefore, the ionic mechanisms that regulate calcium entry into islet cells are critical to maintaining normal glucose homeostasis. Genome wide association studies have identified single nucleotide polymorphisms, including five located in or near ion channel or associated subunit genes, which show association with human diseases characterized by dysglycemia. This review focuses on polymorphisms and mutations in ion channel genes that are associated with perturbations in human glucose homeostasis and discusses their potential roles in modulating pancreatic islet hormone secretion.
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