Liver induction, possible mechanism

More direct interference with glucose metabolism cannot be excluded. Interferon alfa can reduce the sensitivity of peripheral tissues or liver to insulin and accelerate the destruction of stimulated pancreatic beta-cells (540,541) this could be a possible mechanism in patients not exhibiting islet cell antibodies. This is also in keeping with rare instances of induction or exacerbation of type II noninsulin dependent diabetes mellitus (SEDA-19, 335). 

Two widely accepted possible mechanisms for the induction of peroxisome proliferation are (1) activation of specific genes by the chemical or its metabolites, either directly or mediated by a specific receptor, and (2) substrate overload, either as a result of lipolysis occurring outside the liver and causing an influx of fatty acids into the liver or as a consequence of the peroxisome proliferators or their metabolites perturbing lipid metabolism. 

The alternative type of explanation is that the translation of these mENAs is specifically repressed by some mechanism (pres mably through the binding of the mENP proteins) and that their translation requires some sort of cytoplasmic induction. In this case, mobilisation of the mENA into polysomes would not necessarily follow treatment of the cells with low levels of cycloheximide, but would require exposure of the cells to the appropriate inducer. One possible candidate for an inducer may be Fe++ which causes a doubling in the rate of ferritin synthesis in tissue culture cells and in liver (64 65). In the control sitiiation only 50% of the cytoplasmic ferritin mENA in liver is associated with polysomes, and the rest occiirs as free mENPs. Administration of Fe" results in the rapid assimilation of all the ferritin mENA into polysomes (65). If further investigation confirms these results, and shows that Fe selectively controls ferritin mENA translation and has little effect... 

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