FIGURE 2.

Mechanism of Akt at the organ level. As an important regulator of glucose and lipid metabolism, Akt plays a vital role in the occurrence and development of MetS. Abnormalities in Akt in pancreatic β cells, skeletal muscle cells, fat cells, and liver cells, especially the inhibition of Akt expression, lead to a decline in insulin secretion by pancreatic β cells, which affects insulin levels in target cells such as skeletal muscle cells, adipocytes, and liver cells (A). Decreased insulin sensitivity reduces the absorption of glycogen by skeletal muscle cells (B), reduces glycogen synthesis in the liver (C), increases lipolysis, and produces IR. In the visceral obesity model, the Akt-mediated insulin signaling pathway is inhibited, the lipolysis inhibition effect decreases, and the plasma FFA content increases, which in turn induces glucose and lipid metabolism disorders and IR. As a substrate for the synthesis of TGs, FFAs can simultaneously promote the production of VLDL and lead to dyslipidemia (D). The Akt-mediated pathway is one of the core pathways that leads to endothelial dysfunction, which is mostly induced by factors such as IR, visceral fat, FFA elevation, and dyslipidemia. After induction of endothelial dysfunction, these factors can be aggravated, promoting the occurrence and development of MetS (E). Intestinal flora can affect the occurrence and development of MetS by regulating Akt phosphorylation (F).