In Table 1, under Liver,you state: Intact Akt-mTORC1–SREBP-1c signaling → excessive lipogenesis as part of the mechanism of insulin resistance. However, this directly contradicts your own text in Section 3.3.2 (page 13), where you correctly describe selective insulin resistance, i.e., impaired PI3K-Akt signaling but preserved Akt-mTORC1-SREBP-1c. Listing intact lipogenic signaling as an impairment is conceptually wrong. Do you acknowledge that this represents a misunderstanding of selective insulin resistance, and that Table 1 conflates pathophysiology with compensatory mechanisms?
