Adipocytokine signaling pathway in dyslipidemia. Adipocytokines regulate lipid metabolism by inhibiting FAS expression and promoting CPT1 expression. Arrows represent stimulatory modifications. T-shaped arrows represent inhibitory modifications. The picture was generated using Adobe Illustrator CC version 23.0 (Adobe Systems, Inc.). LEP, leptin; LEPR, leptin receptor; JAK2, janus kinase 2; CPT1, carnitine palmitoyl transferase 1; FAS, fatty acid synthase; SREBP-1c, sterol regulatory binding protein-1c; Y, tyrosine.

Adipocytokine signaling pathway in dyslipidemia. Adipocytokines regulate lipid metabolism by inhibiting FAS expression and promoting CPT1 expression. Arrows represent stimulatory modifications. T-shaped arrows represent inhibitory modifications. The picture was generated using Adobe Illustrator CC version 23.0 (Adobe Systems, Inc.). LEP, leptin; LEPR, leptin receptor; JAK2, janus kinase 2; CPT1, carnitine palmitoyl transferase 1; FAS, fatty acid synthase; SREBP-1c, sterol regulatory binding protein-1c; Y, tyrosine.

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Dyslipidemia is an umbrella term for a range of lipid metabolic disorders in the body. This condition has been widely reported to greatly increase the risk of cardiovascular diseases, threatening human health. In recent years, advances in molecular biology have deepened understanding of the dyslipidemia-related signaling pathways and specific mecha...

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... of energy homeostasis, glucose and lipid metabolism (58). In particular, APN and LEP are closely associated with lipid metabolism in the body (59). APN regulates lipid metabolism by activating the AMPK signaling pathway as previously described (32,33). LEP serves a key role in the process of lipid metabolism through a continuous process ( Fig. 5; generated using Adobe Illustrator CC version 23.0; Adobe Systems, Inc.). LEP can bind to its receptor (LEPR) to activate Janus kinase 2 (JAK2), which in turn phosphorylates three tyrosine residues on LEPR (Y985, Y1077 and Y1138) (60). Y1138 then recruits and activates the STAT3 by phosphorylation (60). Subsequently, activated STAT3 ...

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... Molecular biology studies have linked the metabolism and synthesis of lipoprotein to multiple signal transduction pathways, such as protein kinase B (PKB) or AKT, AMPK, SREPB or PPAR. Turning specific pathways on or off can change lipid metabolism and help lower lipid levels (44). Different signaling networks control the body's homeostasis. ...
... The transcription factor FOXO1 promotes the expression of genes that encode for APO C III, which blocks LPL activity, and MTP (Microsomal triglyceride transfer protein), the rate-limiting step in VLDL synthesis. Thus, in addition to lowering plasma LDL levels, stimulation of the AKT pathway also decreases chylomicron and VLDL TG hydrolysis (44). ...
... AMPK influences lipid metabolism through three mechanisms: first, by decreasing the synthesis of Malonyl Co-A via the inactivation of ACC (7,44), malonyl Co-A inhibits CPT1, an enzyme that stimulates FA oxidation in blood; and second, it inactivates FAS by reducing the expression of SREBP 1c. The third route phosphorylates HMGC reductase, the rate-limiting enzyme in cholesterol biosynthesis, rendering it inactive (8). ...