Despite significant weight loss, a lack of improvement in the ability to increase fat oxidation during β-adrenergic stimulation in obese subjects was observed (4), and under similar conditions the ability to increase fat oxidation during exercise in T2D individuals remained impaired (5)
What the above quote should tell you is that obesity is a disease, not simply a matter of "positive energy balance". The primary lesion of obesity ( whatever the hell it is ) is still THERE and causing impairment even after weight loss.
Anyway, this paper is about how serum FFA availability might influence the oxidation of intramyocellular fat. In both lean and obese people, higher levels of serum FFA reduce the oxidation of intramyocellular lipids, so basically, fat delivered to muscle cells from the blood seems to have a higher priority for oxidation than lipid already stored within the muscle cell. This is NOT because of an effect of extracellular lipids on intramyocellular lipolysis.
I was thinking that the association between obesity, diabetes, and ectopic fat deposition might go like this...
fasting hyperinsulinemia -> elevated adipocyte insulin resistance, -> FFA leak -> elevated serum FFA -> reduced intramyocellular lipid oxidation -> increased ecoptic fat storage in muscle.
In the study, they took muscle biopsies from lean and obese T2DM people and cultered them in vitro. The interesting thing is that even in culture, the impaired muscle fat oxidation in the obese peoples cells remains. What this tells you is that it is unlikely ( but not impossible ) that a circulating factor present in obese people is causing the overall reduced fat oxidation, but it suggests the reduced fat oxidation is an intrinsic property of the cell.
An important observation is that when fatty acid availability is high, the oxidation of intracellular lipids is decreased. In general, most fatty acids that are taken up in skeletal muscle are shuttled toward oxidation (Fig. 8A). In subjects with a reduced capacity for lipid oxidation ( i.e. obese people ) , a larger part of the fatty acids taken up may be shuttled toward storage.
When comparing myotubes from obese T2D individuals to lean controls, the oxidation of both intracellular and extracellular lipids was reduced, and the T2D myotubes showed a lower ability to increase extracellular and total lipid oxidation upon increased fatty acid availability.
Anyway, im not a big fan of the mitochondrial disease theory of obesity/T2DM, but the fact that the impaired fat oxidation is preserved when moving from in vivo to in vitro certainly argues for it.
Then again, maybe obesity is just a morale failing. Us fatties just eat too much. If only we had more willpower we could increase our muscle fat oxidation.