The metabolic fate of an oral long-chain-triacylglycerol (LCT) load and of a mixed oral LCT and mediumchain-triacylglycerol (MCT) load was followed for 6 h in eight control and eight obese subjects with normal postabsorptive triacylglycerol concentrations. Labeled triacylglycerol and indirect calorimetry were used. Results showed that LCTs were less oxidized in obese than in control subjects (3.2 ± 0.5 compared with 6.0 ± 0.4 g, P < 0.01). Moreover, the amount of LCT oxidized was negatively correlated with fat mass (r = 20.77, P < 0.01). Appearance in plasma of dietary triacyglycerol-derived long-chain fatty acids was blunted in obese subjects and it was negatively related to fat mass (r = 20.84, P < 0.01) and positively to LCT oxidation (r = 0.70, P < 0.01). On the contrary, MCT oxidation was not altered in obese subjects compared with control subjects. Furthermore, the proportion of MCTs oxidized was higher in both groups compared with LCTs (x – ± SEM: 57.5 ± 2.6% compared with 15.± 1.6%, P < 0.01, n = 16). Our conclusion is that obesity is associated with a defect in the oxidation of dietary LCTs probably related to an excessive uptake by the adipose tissue of meal derived long-chain fatty acids. MCTs, the oxidation of which is not altered in obesity, could therefore be of interest in the dietary treatment of obesity. Am J Clin Nutr 1998;67:595–601
It is important to remember that correlation does not equal causation. The obese tend to have higher circulating lipids and elevated NEFA, and, of course, more fat tissue into which dietary fat can be cleared. It is also important to note that it is the oxidation of diet-derived LCT's that is lower in the obese, not necessarily the oxidation of all endogenous fatty acids. Since the obese also tend to have higher levels of ectopic lipid accumulation (lipids stored in the cells of skeletal muscle and organs such as the liver), these combined observations would seem to be adaptations to the obese state rather than the causes of the obese state.
One can see that chylo-trigs and VLDL responses are similar between obese and non-obese controls. But the free fatty acid levels (the squares/middle curve) rise considerably less in the obese. So it seems that the obese sequester away more dietary fat than the non-obese. Makes sense as the obese have more endogenous fat to "burn".
Since dietary MCT oxidation is not altered, these researchers suggest that they may be of interest in dietary treatment of obesity. Replacing LCT's with MCT's has been shown to promote weight loss in some studies, but I don't believe this is due to differences in utilization of dietary fats for energy. MCT's have slightly fewer calories than LCT's (8 cal/g vs. 9 on average) and MCT's have a higher TEF, so these two combined can improve the caloric balance.
GCBC Fact Check!! This study also demonstrates, yet again, that fat CAN accumulate in the absence of carbohydrate. Interestingly, there was a small but significant insulin spike in the non-obese (those that exhibited MORE lipolysis of dietary fat and subsequent oxidation of those fatty acids), while the insulin response was absent in the obese, who deposited more of their dietary fat intake in their adipose tissue. Exactly the opposite of what Taubes' theories would predict.