Role of K_ATP channels in β‐cell resistance to oxidative stress

Abstract

The importance of K(ATP) channels in stimulus-secretion coupling of β-cells is well established, although they are not indispensable for the maintenance of glycaemic control. This review article depicts a new role for K(ATP) channels by showing that genetic or pharmacological ablation of these channels protects β-cells against oxidative stress. Increased production of oxidants is a crucial factor in the pathogenesis of type 2 diabetes mellitus (T2DM). T2DM develops when β-cells can no longer compensate for the high demand of insulin resulting from excess fuel intake. Instead β-cells start to secrete less insulin and β-cell mass is diminished by apoptosis. Both, reduction of insulin secretion and β-cell mass induced by oxidative stress, are prevented by deletion or inhibition of K(ATP) channels. These findings may open up new insights into the early treatment of T2DM.

Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels

“…It appears interesting to probe this channel site for different types of gasotransmitters and ROS also at BK channels. Other types of K + channels and oxidative stress are discussed in [ 112 , 117 , 237 , 238 ].…”

Inhibition of NF-κB activation improves insulin resistance of L6 cells

“…Apoptosis is a mechanism that contributes to the number decreasing of pancreatic β-cells, which will result in insulin resistance [17]. Pancreas has relatively lower level of antioxidants compared with other organs [18].…”

El tratamiento con testosterona regula positivamente los niveles de proteína y ARNm de la enzima superóxido dismutasa dependiente de Mn en los islotes pancreáticos de ratas macho (Rattus norvegicus)

“…Se ha propuesto que el estrés oxidativo es un elemento clave implicado en el deterioro de la función de las células beta durante el desarrollo de la diabetes tipo 1 y tipo 2 (Domingueti et al, 2016). La pérdida de la función de las células beta, causada por un aumento de la apoptosis y manifestada como una capacidad secretora reducida, es un evento clave en el desarrollo de ambos tipos de diabetes (Drews & Düfer, 2012).…”