I'll just put this up as a brief post, there is a lot of background to it.
We all know that long chain fully saturated fatty acids yield approximately twice as much NADH as FADH2 giving an FADH2:NADH ratio just under 0.5 and that this high rate of FADH2 input at the CoQ couple facilitates superoxide generation by reverse electron transport through complex I.
Equally, we know that glucose oxidation, with five times the generation of NADH as FADH2, gives us a ratio of 0.2 and minimal reverse electron transport
We also know that, in order to balance the cytosolic NAD+:NADH ratio that NADH must be converted back to NAD+ to allow glycolysis to continue. This can be done using the malate-aspartate shuttle, conversion of pyruvate to lactate (both of which are redox neutral) or by using the glycerophosphate shuttle.
The latter is far from redox-neutral from the FADH2 input perspective. A cytoplasmic NADH is converted to an FADH2 within mtG3Pdh. This inputs at the CoQ couple. As far as the mitochondria are concerned that cytoplasmic NADH never existed. It behaves exactly as an FADH2. So, while the glycerophosphate shuttle is active, glucose presents to the mitochondria as two FADH2 and four NADH, giving us a nice, rather neat, FADH2:NADH ratio of 0.5. Slightly higher than palmitate or stearate.
I consider the glycerophosphate shuttle as generating essential ROS for insulin signalling. Small amounts of ROS generation facilitates insulin signalling. Large amounts inhibit it. Glucose, even hyperglycaemia, dose not generate ROS by the RET route. Adding insulin does do so because as the pyruvate dehydrogenase complex becomes more active then so the glycoerophosphate shuttle also becomes more active. The FADH2:NADH from glucose rises from 0.2 towards 0.5 and ROS increase to generate (given enough activation of the PDH complex) insulin resistance.
Insulin induced insulin resistance.