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(1999b)

Reports that newborns with a complete lack of insulin effects due to inactivating defects in the INSR gene can now survive for extended time into adolescence when treated with recombinant IGF-I, that stimulate glucose uptake via the IGF1R sharing common signaling pathways with the INSR, support an important direct role of IGF-1 signaling on metabolism (93)

this pathway will, in turn, upregulate pro-fibrogenic matrix metalloproteinase-2 (MMP2) and downregulate matrix metalloproteinase-1 (MMP1), two enzymes responsible for remodeling the hepatic extracellular matrix [9, 191, 192, 216]

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