Figure 5
A scheme which pictures the function of the SUR1/KIR.2.6 potassium channel in pancreatic β-cells—in a physiological state (4a and 4b), and in the case of the gain-of-function mutation, hypothesized to be caused by SARS-CoV-2. Upon polarization of the cell membrane, K+ are released through KATP to the extracellular fluid (Fig. 3a). An increase in glycemia induces the shutting of the KATP and increasing the intracellular concentration of ATP and Ca2+, inducing membrane depolarization and insulin secretion (Fig. 4b). The mutations in genes coding for SUR1 or KIR.2.6 activate the KATP channel, preventing the closure of the KATP channel, regardless of glycemia. These mutations prevent insulin secretion, consequently promoting hyperglycemia (similarly to the pathomechanism of MODY diabetes).
