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doi: 10.1007/s00018-017-2496-y 98 MignattiPRifkinDB
Finger, B
2022;5:e202101157
Most of the intestine-on-chip models developed so far have been based on immortalized cell lines (123, 138140)
Hu D, Li Y, Li R, Wang M, Zhou K, He C, Wei Q, Qian Z
Taking all this data together it seems logical or appropriate to conclude that, because IGF1-R has a different signalling pathway that can maintain lipid oxidation in the liver, FFA uptake in muscle, and activates mTORC1 could reactivate IR through tyrosine kinase activity on IRS, thus displacing serine phosphorylation, reinstituting insulin signalling
