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doi: 10.1038/ncpneuro0148 [DOI] [PubMed] [Google Scholar] 105

Additionally, obesity and IR both contribute to -cell dysfunction and apoptosis, mechanistically explained by glucotoxicity and increased immunogenicity (the accelerator hypothesis) or by -cell exhaustion due to increased metabolic demand (the overload hypothesis) [23]

In addition, NMDAR-mediated intracellular Ca 2+ signals could modulate gene expression and thereby drive the down-regulation of K v 4.2, K v 4.3, K v 11.1, and KChIP2 [41], as well as SERCA2a [43] and proteins (Figure 3B)

For instance, the CPSG motif was observed to be less efficient in facilitating this reaction