FATP1Fatty Acid Transport Protein 1
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Lally et al., "Increasing skeletal muscle fatty acid transport protein 1 (FATP1) targets fatty acids to oxidation and does not predispose mice to diet-induced insulin resistance," Diabetologia, vol.
FATPs have been shown to be expressed in a variety of tissues [49], and of particular importance is the expression of the murine FATP1 and FATP4 in the brain [49].
In addition to exploring FATP1 and FATP4, investigating pathways involved in regulating transcription of antiapoptotic genes was another objective.
After investigating these pathways it was determined that the neuroprotective mechanisms of VEGF-B involve upregulation of FATP1 and FATP4 and activation of Akt and Erk1/2 signaling pathways.
In summary, it was shown that the mechanisms of VEGFB's neuroprotective action can involve VEGFR-1 mediated upregulation of FATP1 and FATP4 and activation of the Akt and Erk 1/2 signaling pathways [19] (Figure 1).
On the other hand, as observed in T2DM patients, a decline of cardiac function and increased myocardial hypertrophy, fibrosis, and steatosis were predominantly found in PPAR[alpha] [105, 106], PPAR[gamma] [107, 108], long-chain acyl-CoA synthetase-1 (LCACS1) [109, 110], lipoprotein lipase (LPL) [111, 112], and fatty acid transport protein-1 (FATP1) [113, 114] overexpressed mice.
Moreover, ATGL, LPL, and FATP1 are involved in FA uptake and accumulation in the cardiomyocytes, and LCACS1 catalyses the first step of lipid biosynthesis.