The dysfunctional mitochondria notion is enticing, but blown out of the water by the works of Holoszy's group, for example: http://www.pnas.org/content/105/22/7815.full.pdf
My blog post on that study: http://carbsanity.blogspot.com/2011/09/mitochondria-and-high-fat-diets.html
From the paper: It is surprising that the mitochondrial deficiency causes insulin resistance concept has been so widely accepted, because it seems untenable in the context of what is known regarding the capacity of skeletal muscle for oxidative metabolism. The mechanism by which a 30% decrease in muscle mitochondria has been proposed to cause muscle insulin resistance is an impairment in the ability to oxidize fat, resulting in accumulation of intramyocellular lipids (1, 2). Actually, the rate of substrate oxidation in resting muscle is not determined/limited by mitochondrial oxidative capacity but by the rate of ATP breakdown/ADP formation, which is regulated by the cells’ need for energy (39). The energy/substrate requirement of resting muscle cells is determined by ‘‘housekeeping’’ functions, such as maintenance of transmembrane potential by the Na/K ATPase, protein synthesis, etc., and is very low relative to the maximal capacity of muscle for substrate oxidation. Increasing the supply of FFA or glucose to resting muscle can change the relative proportions of these substrates that are oxidized but does not result in an
increase in substrate oxidation above that required to supply the energy needed for ATP repletion, regardless of its content of mitochondria.
As regards Peter's contention: "Fatty acid uptake is (predominantly) controlled at the mitochondrial surface." Actually FA's pass two membranes to be oxidized. Uptake into the cell from circulation and uptake across the mitochondrial membrane once inside the cell. Different mechanisms are involved in each. So, I'm not sure where he gets this definitive statement from.
The adipocyte balloon? A left-over of the part of Taubes' misinformation on the progression of insulin resistance. The overwhelming scientific evidence is that systemic, pathological insulin resistance begins in the fat tissue.
The "Rogge hypothesis" (http://brn.sagepub.com/content/10/4/356.full.pdf) does not meet the initial test of explaining the epidemic of obesity. She implies that some underlying mitochondrial defect results in excess glucose metabolism at the expense of fatty acid oxidation and this is alleviated by increasing intake to increase fat stores. So that when obese folks re-establish a "normal" RQ. Only they don't ... the obese are better fat burners according to their very low RQ. Dysfunctional mitochondria? In the Ranneries study where the formerly obese had a higher resting RQ, the RQ during activity was indistinguishable between groups (http://carbsanity.blogspot.com/2011/10/fat-metabolism-in-formerly-obese-women_06.html). Rogge's cites conflict with Ranneries' results. From the Rogge paper:
In a study of the effects of dietary-induced weight loss in obese adults, weight loss did not alter the overall percentage of energy derived from fat (47%) under resting conditions, but the amount of energy derived from fat in the 5-hr postmeal period was severely depressed. At baseline, obese participants derived 38% of total energy expenditure from fat during the postmeal period; following weight loss, the participants obtained only 26% of their total energy from fat oxidation (Ballor, Harvey-Berino, Ades, Cryan, & Calles-Escandon, 1996). These results are in agreement with the findings of a study comparing the resting and postprandial energy expenditure and substrate use for reduced-obese, weight-stable women and never-obese women (Raben et al., 1994). The two groups of women had no significant differences in their resting energy expenditure or in their use of energy substrates. However, the formerly obese women exhibited a reduction in fat oxidation twice as great as that of the never-obese women following a high-fat meal. In addition, the rate of carbohydrate oxidation was significantly higher among the formerly obese women.
So? The FO burned more carb and less fat. They didn't burn a different amount of total energy. It's ultimately about energy balance. You need the ATP you need. Your body can get it from glucose, fatty acids, amino acids and ketones. This whole mitochondrial dysfunction tangent is getting folks nowhere. But I suppose it is a good face-saving diversion for those who believed Peter when he kept insisting that fasting insulin levels determine weight loss.