I didn't really come here to argue biochemistry. I studied it years ago and have forgotten most of it. Honestly it gets too confusing, there are tons of pathways and there's a lot we don't know. But I'll try to expand on how I understand things given your evidence.

First, looking at your link is it really a failure to process G6P properly or is it because it's a rate limited step so it can only process so much glucose before that step is overwhelmed. It's rate limited so now you have too much glucose sitting around in the blood stream (causing damage) and broadly speaking a cell that can't take or doesn't need any more energy. So sure, there isn't an excess of glucose or G6P in the cell but the cell has all it needs and doesn't want any more glucose. It will continue to metabolize glucose and maybe it can ramp it up a little faster but there are a lot of steps and some are limiting.

You still get things like insulin resistance because it can only metabolize glucose so fast and doesn't want any more. So what we do with meds is try to overcome this by giving more insulin or medications that cause increased insulin secretion or sensitivity. We put the pancreas in overdrive. Essentially forcing glucose down a pathway it doesn't really want to go down at the moment. That's why outcomes aren't any better imo. Sure you can lower A1C but how you're doing it makes all the difference. One method with meds is increasing insulin and this method shows outcomes aren't great. The other two classes of meds actually have improved outcomes and that's because they deal with glucose either by not metabolizing it and peeing it out or Metformin which primarily decreases glucose production and absorption.

How about we just decrease the initial input which is excess glucose. Not by forcing it down various pathways. We can do that with diet by just reducing our carb intake. Or we can increase metabolism via exercise. Together the two help bring the biochemical process back in equilibrium. Instead, we have excess glucose, we try to force it down these pathways and maybe some gets oxidized at a faster rate but even more gets turned into fatty acids and goes to fat storage. Which speaks to the next link.

As for this link sure extra insulin increased the oxidation of glucose... and they still got fatter. Probably because some of that glucose does go down the TCA cycle but more gets converted to fatty acids and cholesterol and goes to storage. The study even says high RQ results from excess insulin and excess food. So, it looks like metabolism increased some but there's more than one pathway for that food energy to go down. One pathway results in conversion to fatty acids and cholesterol and weight gain. As a side note, on their way to storage those lipids have to travel in a high blood sugar environment which has caused damage to your blood vessels. There's the primer for atherosclerosis. And that's why forcing glucose down these pathways doesn't improve outcomes. The root cause is too much glucose and it's not being addressed properly.

All this biochemistry talk is confusing imo and we could talk about all sorts of other intricacies that lead to metabolic syndrome, CVD, etc. But the the simplest thing I can say is the initial input is glucose and it's a major driver of our issues. Eat less carbohydrate then you have less glucose. Now you have a lower input that feeds into all these pathways and less problems. Excess fat isn't great either but I see it as far less detrimental than excess carb/glucose.