1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters. 2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters. 3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.