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However, the accumulated data suggest that the overactivation of this signaling system could stem from inactivation or genetic ablation of the tuberous sclerosis complex (TSC) [261, 262], the master negative regulator of mTOR
These genes may participate in shared regulatory pathways related to HFHFD-induced metabolic dysfunction and the therapeutic actions of semaglutide and tirzepatide
In particular, while several studies suggest that -3 PUFA consumption has protective effects on the development of autoimmune thyroiditis [122], others demonstrate that exposure to pollutants (especially heavy metals) that contaminate fish is associated with an increased risk of autoimmunity and thyroid dysfunction [121,124,125,126]
doi: 10.3389/fbioe.2021.677576
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