Mechanism of Free Fatty Acid–induced Insulin Resistance in Humans

Mechanism of Free Fatty Acid–induced Insulin Resistance in Humans  (PDF)

these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an ~50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.

The introduction section discusses the history and controversy over how NEFA/FFA induce insulin resistance.  

In conclusion, contrary to the classical mechanism of free fatty acid–induced insulin resistance as proposed by Randle et al. (2, 27, 28) in which free fatty acids exert their effect through initial inhibition of pyruvate dehydrogenase, we found that elevation in plasma free fatty acid concentration causes insulin resistance by inhibition of glucose transport and/or phosphorylation with a subsequent reduction in rates of glucose oxidation and muscle glycogen synthesis. This reduction in insulin inducible glucose transport/phosphorylation is similar to what is observed in patients with NIDDM (20) and their normoglycemic-insulin–resistant offspring (24) and suggests that alterations in intramuscular FFA metabolism may play an important role in the pathogenesis of the insulin resistance observed in patients with NIDDM.

I'm not sure this study presents any "final word" on this, but it's not the carbs in the Western diet that lead to  insulin resistance.  Perhaps it could be said that the increase in obesity, IR and Type 2 diabetes in Western countries is due to seeing the effect of the IR due to increased carb consumption.  Insulin resistance is not caused by high insulin spikes or basal levels, it is the instigator of higher insulin spikes in response to carbs/proteins.