PDF(Pubmed)
Abstract：
Ionic channels are present in eucaryotic plasma and intracellular membranes. They coordinate and control several functions. Potassium channels belong to the most diverse family of ionic channels that includes ATP-dependent potassium (KATP) channels in the potassium rectifier channel subfamily. These channels were initially described in heart muscle and then in other tissues such as pancreatic, skeletal muscle, brain, and vascular and non-vascular smooth muscle tissues. In pancreatic beta cells, KATP channels are primarily responsible for maintaining the membrane potential and for depolarization-mediated insulin release, and their decreased density and activity may be related to insulin resistance. KATP channels\' relationship with insulin resistance is beginning to be explored in extra-pancreatic beta tissues like the skeletal muscle, where KATP channels are involved in insulin-dependent glucose recapture and their activation may lead to insulin resistance. In adipose tissues, KATP channels containing Kir6.2 protein subunits could be related to the increase in free fatty acids and insulin resistance; therefore, pathological processes that promote prolonged adipocyte KATP channel inhibition might lead to obesity due to insulin resistance. In the central nervous system, KATP channel activation can regulate peripheric glycemia and lead to brain insulin resistance, an early peripheral alteration that can lead to the development of pathologies such as obesity and Type 2 Diabetes Mellitus (T2DM). In this review, we aim to discuss the characteristics of KATP channels, their relationship with clinical disorders, and their mechanisms and potential associations with peripheral and central insulin resistance.
摘要：
离子通道存在于真核血浆和细胞内膜中。它们协调和控制多个功能。钾通道属于最多样化的离子通道家族，包括钾整流通道亚家族中的ATP依赖性钾（KATP）通道。这些通道最初在心肌中描述，然后在其他组织如胰腺中描述，骨骼肌,大脑,血管和非血管平滑肌组织。在胰腺β细胞中，KATP通道主要负责维持膜电位和去极化介导的胰岛素释放，它们的密度和活性降低可能与胰岛素抵抗有关。KATP通道与胰岛素抵抗的关系开始在胰腺外β组织如骨骼肌中进行探索，其中KATP通道参与胰岛素依赖性葡萄糖再捕获，它们的激活可能导致胰岛素抵抗。在脂肪组织中，含有Kir6.2蛋白亚基的KATP通道可能与游离脂肪酸和胰岛素抵抗的增加有关；因此，促进脂肪细胞KATP通道抑制延长的病理过程可能导致胰岛素抵抗导致的肥胖。在中枢神经系统中，KATP通道激活可以调节外周血糖并导致脑胰岛素抵抗，早期外周改变，可导致肥胖和2型糖尿病（T2DM）等病理的发展。在这次审查中,我们的目的是讨论KATP通道的特点，它们与临床疾病的关系，及其与外周和中枢胰岛素抵抗的机制和潜在关联。
