So adaptation switches it around. Note how pp insulin gets cut in half for CRD (low-carb). Post-prandial insulin is special because normally the bulk gets sucked up by the liver before we can measure it at the arm. Since there was a big drop for the CRD group, it follows that the liver became very insulin sensitive.

My paradigm explains this by an increase in ketones, where ketones activate insulin receptors. There's little to no ketones in the LFD group, so there's no insulin receptor activation, hence the very small drop comparatively. Also, dietary fat activates the PPAR-a pathway in the liver, which then activates insulin-degrading enzyme, ultimately resulting in a greater capacity to degrade insulin once it hits the liver. After twelve weeks of adaptation to just these two mechanisms meal after meal, a single high-fat meal challenge is no longer a big deal.

Since it's the same high-fat meal challenge for both groups, the insulin response from the pancreas should be the same too. But since there's both a greater capacity to receive insulin by the liver and greater capacity to degrade this insulin due to 12 weeks of high-fat meals, the insulin measured at the arm has already been cut in half by the liver compare to the LFD group.

Besides dietary fat, I suspect fat-solubles, especially vitamin A since it's stored in the liver, play a central role in all this.

Forgot. Why is it more kinda sorta steady-state for the LFD group? Simple. There's always more insulin everywhere.