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Thats short enough to make sustained IGF-1 receptor activation difficult to study in vivo

It is possible that TLR2 signaling or other factors inhibit mTORC1 activation, which leads to autophagy induction and M2 polarization

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The altered glucose flux suppresses the delivery of pyruvate and nicotinamide adenine dinucleotide+ hydrogen (NADH) to the mitochondria, thereby contributing to mitochondrial depolarization by starving mitochondria of energy substrate (Strmland et al

Raff MC, Miller RH, Noble M

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