Sort of why I used the "subtype" ahead of insulin resistance. Insulin does this, that, and the other. When insulin resistance is suggested as, insulin resistance-->increased insulin at subcutaneous fat (or visceral for that matter)-->increased fat, the assumption is that the tissue is still responsive to the fattening effect of insulin. Here I was sort of referring to whether the liver would be responsive to insulin's effect on ldl uptake specifically.

Another effect of insulin is the production of VLDL. Sometimes when type II's first go on insulin, they'll have a reversal of fatty liver--this is because insulin resistance kept them from repackaging triglycerides as VLDL for export. The liver taking in ldl cholesterol, partly because it needs raw material for vldl production probably makes sense.

One thing I wonder about. A lot of us went around for decades with insulin probably considerably higher than it is now. So we've got this cholesterol transport system, used to very high insulin levels. Bring insulin down to normal, even ideal levels, and things don't always go to what's normal and ideal--an example is the problems with electrolytes people can experience. If some of the activities of insulin normalize, but some don't, maybe we get these little weirdnesses.