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首页> 外文期刊>Cell metabolism >Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granules.
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Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granules.

机译：慢性棕榈酸酯暴露通过从分泌颗粒解离Ca（2+）通道抑制胰岛素分泌。

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摘要

Long-term (72 hr) exposure of pancreatic islets to palmitate inhibited glucose-induced insulin secretion by >50% with first- and second-phase secretion being equally suppressed. This inhibition correlated with the selective impairment of exocytosis evoked by brief (action potential-like) depolarizations, whereas that evoked by long ( approximately 250 ms) stimuli was unaffected. Under normal conditions, Ca(2+) influx elicited by brief membrane depolarizations increases [Ca(2+)](i) to high levels within discrete microdomains and triggers the exocytosis of closely associated insulin granules. We found that these domains of localized Ca(2+) entry become dispersed by long-term (72 hr), but not by acute (2 hr), exposure to palmitate. Importantly, the release competence of the granules was not affected by palmitate. Thus, the location rather than the magnitude of the Ca(2+) increase determines its capacity to evoke exocytosis. In both mouse and human islets, the palmitate-induced secretion defect was reversed when the beta cell action potential was pharmacologically prolonged.
机译：胰腺胰岛长期（72小时）暴露于棕榈酸酯可抑制葡萄糖诱导的胰岛素分泌，其> 50％受到抑制，而第一阶段和第二阶段的分泌均被同样抑制。这种抑制作用与短暂（动作电位样）去极化引起的胞吐作用的选择性损伤有关，而长（约250 ms）刺激引起的抑制作用则不受影响。在正常情况下，由短暂的膜去极化引起的Ca（2+）流入将[Ca（2 +）]（i）增加到离散微域内的高水平，并触发紧密相关的胰岛素颗粒的胞吐作用。我们发现，这些区域的局部Ca（2+）进入变得长期（72小时），而不是由急性（2小时），暴露于棕榈酸酯分散。重要的是，颗粒的释放能力不受棕榈酸酯的影响。因此，Ca（2+）增加的位置而不是大小决定了它引起胞吐作用的能力。在小鼠和人类的胰岛中，药理学上延长了β细胞的动作电位后，棕榈酸酯诱导的分泌缺陷得以逆转。

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