First of all, let me say that using rats is somewhat questionable as it is not clear that rat diets are similar to human diets. This is key because if rats are not intended to live off of protein and fat, as I believe humans are, then it wouldn't be surprising to see that such things muck up their systems. It is as questionable as testing the lipid hypothesis of cardiovascular disease on rabbits (which it was).
That being said, I read that study as supporting exactly what I'm saying.
"Therefore, in skeletal muscle of rats, 1) feeding a diet high in fat induces a reduction in
insulin-stimulated glucose uptake but 2) provides an
increase in basal glucose uptake."
So glucose uptake into skeletal muscle increased, but insulin-dependent glucose uptake decreased in the high-fat diet. This means that more glucose found its way into the muscles but that less insulin was needed to get it there. In other words, insulin sensitivity increased. We'd expect the exact opposite if the high-fat diet increased insulin resistance (i.e., less glucose in muscle and more insulin needed to get in there).
Other pertinent statements:
"2-deoxyglucose uptake in HF-mixed-fed rats
did not differ from that in HCHO-fed rats (P > 0.05)."
"Glucose tolerance was significantly reduced in HF-saff-fed rats but was
unaffected by the HF-mixed diet."
"
Insulin-stimulated 3-O-methylglucose uptake into perfused hindlimb muscles was reduced in rats fed HF-saff and HF-mixed diets compared with those fed HCHO diet (P < 0.02)."
Again, it looks like the same amount of glucose found its way into muscles in the mixed high-fat diet, but that less insulin was needed to get it there. This does not, in my mind, spell "insuling resistance." This strikes me as the ideal situation: Plenty of glucose in the muscles, but little insulin output. Sign me up!