Reply to P Schrauwen et al

Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808

Dear Sir:

We are pleased that Schrauwen et al considered our article (1) significant enough to comment on the findings. Our study confirmed and, importantly, extended the work of Schrauwen et al (2) on the time course of adaptation to high-fat diets. The overall implication of our work is 2-fold. First, our results show that individuals are highly variable in their ability to switch off carbohydrate oxidation and increase fat oxidation when exposed to a high-fat diet under isoenergetic conditions. Second, we showed that physical fitness and fasting insulin were predictors of an individual's ability to oxidize dietary fat.

The main concern of Schrauwen et al was that our subjects were in positive energy balance and that this confounded our interpretations. This argument assumes that carbohydrate stores drive fat oxidation. Schrauwen et al's previous results (3, 4), based on the use of exercise as a maneuver to deplete glycogen stores, although confounded, generally support this argument. Contrary to their expectations, energy balance and fat balance in our study were not related. Therefore, the slightly positive energy balance in our study, averaging 1000kJ/d (250 kcal/d), cannot account for the observed relations. This observation was noted clearly at the end of the Results section of the article. The subjects in the study by Abbott et al (5), which was cited to support this relation, had energy balances ranging from -3084 to 1958 kJ (–737 to 468 kcal)/d (5). This range of energy balance was clearly greater than what we observed.

Similarly, Schrauwen et al argued that physically fit volunteers [ie, those with a high maximal oxygen uptake ( Regarding the degree to which we were able to maintain energy balance, there are 2 important points to consider. First, in contrast with the protocols of Schrauwen et al, we directly measured both energy intake (duplicate meals) and fecal energy (bomb calorimetry). Accordingly, we avoided the errors inherent when metabolizable energy and dietary intakes are not directly measured. These 2 measured values obviously cannot be obtained during the conduct of the trial. When we used nutrient database values during the conduct of the study, as did Schrauwen et al, our energy balances were also essentially zero.

Last, Schrauwen et al failed to place our results in the context of other existing literature. In rats fed a high-fat diet, skeletal muscle oxidative capacity (6) and insulin sensitivity (7) were predictors of weight gain during high-fat feeding. These results are strikingly similar to our own.

In summary, the concerns of Schrauwen et al are not borne out by our data. Our ability to approach energy balance by using robust measures of energy intake, nonmetabolizable energy output, and indirect calorimetry was one of the major strengths of our investigation. We are confident in our results, which suggest that physical fitness and insulin sensitivity are important predictors of fat balance during acute high-fat feeding.

REFERENCES

1. Smith SR, de Jonge L, Zachwieja JJ, et al. Fat and carbohydrate balances during adaptation to a high-fat. Am J Clin Nutr 2000;71:450–7.
2. Schrauwen P, Marken Lichtenbelt WDV, Saris WH, Westerterp KR. Changes in fat oxidation in response to a high-fat diet. Am J Clin Nutr 1997;66:276–82.
3. Schrauwen P, Marken Lichtenbelt WDV, Saris WHM, Westerterp KR. Role of glycogen-lowering exercise in the change of fat oxidation in response to a high-fat diet. Am J Physiol 1997;273:E623–9.
4. Schrauwen P, Marken Lichtenbelt WDV, Saris WHM, Westerterp KR. Fat balance in obese subjects: role of glycogen stores. Am J Physiol 1998;274:E1027–33.
5. Abbott WG, Howard BV, Christin L, et al. Short-term energy balance: relationship with protein, carbohydrate, and fat balances. Am J Physiol 1988;255:E332–7.
6. Gayles EC, Pagliassotti MJ, Prach PA, Koppenhafer TA, Hill JO. Contribution of energy intake and tissue enzymatic profile to body weight gain in high-fat-fed rats. Am J Physiol 1997;272:R188–94.
7. Pagliassotti MJ, Horton TJ, Gayles EC, Koppenhafer TA, Rosenzweig TD, Hill JO. Reduced insulin suppression of glucose appearance is related to susceptibility to dietary obesity in rats. Am J Physiol 1997;272:R1264–70.