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When expressed in cultured cells, these mutated proteins can slow the dynamics of SGs and other RNP assemblies, leading to persistent TDP43+ granules and/or the formation of rigid, amyloid-like solids reminiscent of those observed in affected tissues of patients with MSP and related disorders ( 26 31 )

This disruption inhibits GLUT4 membrane translocation, exacerbating insulin resistance (56)

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For example, altered levels of short-chain ACs, including C2 and C3, have been observed in coronary artery disease and diabetes [6, 55]

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