Edit: I no longer think this first paragraph is correct, there is an update here. End edit.
We appear to have two basic states of the electron transport chain. There is the situation under fasting or ketogenic dieting conditions. Here delta psi is low, complex I throughput is low and there is plenty of FADH2 input through electron transporting flavoprotein dehydrogenase coming from the first step of beta oxidation of real fats, like palmitic acid. With a low delta psi it is near impossible to generate reverse electron flow through complex I so activation of insulin signalling is rapidly aborted by the continuing action of tyrosine phosphatase.
This is the insulin resistance of starvation. Without it death from hypoglycaemia would be routine after a day or so without food.
Next is the state of the electron transport chain proteins under the influence of insulin signalling. How this is achieved is currently outside my reading but I think it is perfectly reasonable to assume that specific electron transport chain proteins will be phosphorylated as a direct result of insulin signalling being active. With a large supply of NADH to complex I and a restricted supply of fatty acids due to insulin acting on adipocytes there is a high membrane voltage, high throughput of electrons down the ETC via complex I but no reverse flow because there is a minimal input via electron transporting flavoprotein dehydrogenase's FADH2.
These are the two simple extremes of organisation under "isocaloric" conditions and neither generates significant reverse electron flow, ie there is minimal superoxide production at complex I.
Under hypercaloric conditions, usually an elevated supply of both glucose and fatty acids, we have the high delta psi, high FADH2 input through electron transporting flavoprotein dehydrogenase from beta oxidation and so significant reverse electron flow through complex I to signal that more than enough calories are available to the cell.
Under simple glucose based caloric overload mtG3P dehydrogenase steps in in the place of electron transporting flavoprotein dehydrogenase and supplies an FADH2 input to signal the need for hypercaloric insulin resistance. This seems a perfectly reasonable approach to hyperinsulinaemic hyperglycaemia.
Under normal physiology I would expect blood glucose to remain under 7mmol/l at all times, probably under 6mmol/l, provided the food eaten is food and the physiology processes used are undamaged. Even under caloric overload with a baked spud.
What do we really mean by caloric overload?
Overload is the utterly normal response to eating any meal. ANY meal. As soon as the rate of calorie absorption exceeds the post prandial metabolic requirement, we need to store the excess calories. The development of individual cell insulin resistance is utterly normal under these conditions. Blood glucose, blood lipids and blood insulin rise. Fat is diverted to adipocytes. Glucose is diverted to glycogen stores.
All of this is achieved by reverse electron flow through complex I generating a physiological response. The acute storing of calories is essential. This is how we do it.
The diversion of glucose to the brain in starvation is induced by failure to sustain insulin activation due to lack of sufficient mitochondrial membrane potential needed to signal that it's OK to respond to insulin. Low insulin is helpful and low glucose is essential for this process.
I think this summarises the Protons thread to date.
Perhaps we can go on to look at some pathology sometime. Mix 'n' match of the two situations is not a good idea.