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The relevance of AMP-activated protein kinase in insulin-secreting β cells: a potential target for improving β cell function?
Journal of Physiology and Biochemistry ( IF 3.7 ) Pub Date : 2019-11-05 , DOI: 10.1007/s13105-019-00706-3
Tomasz Szkudelski 1 , Katarzyna Szkudelska 1
Affiliation  

AMP-activated protein kinase (AMPK) is present in different kinds of metabolically active cells. AMPK is an important intracellular energy sensor and plays a relevant role in whole-body energy homeostasis. AMPK is activated, among others, in response to glucose deprivation, caloric restriction and increased physical activity. Upon activation, AMPK affects metabolic pathways leading to increased formation of ATP and simultaneously reducing ATP-consuming processes. AMPK is also expressed in pancreatic β cells and is largely regulated by glucose, which is the main physiological stimulator of insulin secretion. Results of in vitro studies clearly show that glucose-induced insulin release is associated with a concomitant inhibition of AMPK in β cells. However, pharmacological activation of AMPK significantly potentiates the insulin-secretory response of β cells to glucose and to some other stimuli. This effect is primarily due to increased intracellular calcium concentrations. AMPK is also involved in the regulation of gene expression and may protect β cells against glucolipotoxic conditions. It was shown that in pancreatic islets of humans with type 2 diabetes, AMPK is downregulated. Moreover, studies with animal models demonstrated impaired link between glucose and AMPK activity in pancreatic islet cells. These data suggest that AMPK may be a target for compounds improving the functionality of β cells. However, more studies are required to better elucidate the relevance of AMPK in the (patho)physiology of the insulin-secreting cells.

中文翻译:

AMP激活的蛋白激酶在分泌胰岛素的β细胞中的相关性:改善β细胞功能的潜在目标?

AMP激活的蛋白激酶(AMPK)存在于不同种类的代谢活性细胞中。AMPK是重要的细胞内能量传感器,在全身能量稳态中起着重要的作用。响应于葡萄糖缺乏,热量限制和身体活动增加,AMPK被激活。激活后,AMPK影响代谢途径,导致ATP形成增加,同时减少ATP消耗过程。AMPK也表达于胰腺β细胞中,并在很大程度上受葡萄糖的调节,葡萄糖是胰岛素分泌的主要生理刺激剂。体外研究结果清楚地表明,葡萄糖诱导的胰岛素释放与β细胞中AMPK的伴随抑制有关。然而,AMPK的药理激活显着增强了β细胞对葡萄糖和其他刺激的胰岛素分泌反应。该作用主要是由于细胞内钙浓度增加。AMPK还参与基因表达的调节,并可能保护β细胞免受糖脂毒性条件的侵害。结果表明,在患有2型糖尿病的人的胰岛中,AMPK被下调。此外,动物模型研究表明,胰岛细胞中葡萄糖和AMPK活性之间的联系受损。这些数据表明,AMPK可能是改善β细胞功能的化合物的靶标。但是,需要更多的研究来更好地阐明AMPK在胰岛素分泌细胞的(病理)生理学中的相关性。该作用主要是由于细胞内钙浓度增加。AMPK还参与基因表达的调节,并可能保护β细胞免受糖脂毒性条件的侵害。结果表明,在患有2型糖尿病的人的胰岛中,AMPK被下调。此外,动物模型研究表明,胰岛细胞中葡萄糖和AMPK活性之间的联系受损。这些数据表明,AMPK可能是改善β细胞功能的化合物的靶标。然而,需要更多的研究来更好地阐明AMPK在胰岛素分泌细胞的(病理)生理学中的相关性。该作用主要是由于细胞内钙浓度增加。AMPK还参与基因表达的调节,并可能保护β细胞免受糖脂毒性条件的侵害。结果表明,在患有2型糖尿病的人的胰岛中,AMPK被下调。此外,动物模型研究表明,胰岛细胞中葡萄糖和AMPK活性之间的联系受损。这些数据表明,AMPK可能是改善β细胞功能的化合物的靶标。然而,需要更多的研究来更好地阐明AMPK在胰岛素分泌细胞的(病理)生理学中的相关性。结果表明,在患有2型糖尿病的人的胰岛中,AMPK被下调。此外,动物模型研究表明,胰岛细胞中葡萄糖和AMPK活性之间的联系受损。这些数据表明,AMPK可能是改善β细胞功能的化合物的靶标。然而,需要更多的研究来更好地阐明AMPK在胰岛素分泌细胞的(病理)生理学中的相关性。结果表明,在患有2型糖尿病的人的胰岛中,AMPK被下调。此外,动物模型研究表明,胰岛细胞中葡萄糖和AMPK活性之间的联系受损。这些数据表明,AMPK可能是改善β细胞功能的化合物的靶标。然而,需要更多的研究来更好地阐明AMPK在胰岛素分泌细胞的(病理)生理学中的相关性。
更新日期:2019-11-05
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