Background: Adjustments of carbohydrate intake and oxidation occur in both normal-weight and overweight individuals. Nevertheless, the contribution of carbohydrates to the accumulation of fat through either reduction of fat oxidation or stimulation of fat synthesis in obesity remains poorly investigated.
Objective: The objective of this study was to assess the postprandial metabolic changes and the fractional hepatic de novo lipogenesis (DNL) induced by a high-carbohydrate, low-fat meal in lean and overweight young men.
Design: A high-carbohydrate, low-fat meal was administered to 6 lean and 7 overweight men after a 17.5-h fast. During the fasting and postprandial periods, energy expenditure (EE), macronutrient oxidation, diet-induced thermogenesis, and serum insulin, glucose, triacylglycerol, and fatty acids were measured. To determine DNL, [1-13C]sodium acetate was infused and the mass isotopomer distribution analysis method was applied. **My addition: Subjects were fed isocaloric diet for 3 days prior to ensure equivalent glycogen stores.
Results: After intake of the high-carbohydrate meal, the overweight men had hyperinsulinemia and higher fatty acid and triacylglycerol concentrations than did the lean men. The overweight group showed a greater EE, whereas there was no significant difference in carbohydrate oxidation between the groups. Nevertheless, the overweight men had a marginally higher protein oxidation and a lower lipid oxidation than did the lean men. DNL was significantly higher before and after meal intake in the overweight men and was positively associated with fasting serum glucose and insulin concentrations. Furthermore, postprandial DNL was positively correlated with body fat mass, EE, and triacylglycerol.
Conclusion: After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional hepatic fat synthesis than did lean men.
The discussion section is of great interest to me, especially as relates to the claim that it is excess carbs that are turned to fat. Some excerpts:
It is known that dietary carbohydrate promotes its own oxidation (9, 13, 32) and that under normal conditions DNL is not a major way to increase body fat stores, as found by other investigators using indirect calorimetry (20, 31). Most short-term studies (13–15, 30) in which carbohydrate was added to mixed diets, even in large quantities, did not show net DNL, based on indirect calorimetry, because storage as glycogen was concluded to represent the fate of excess dietary carbohydrate. In the present study, NPRQ was high throughout the postprandial period, reaching values slightly >1 in the overweight group after the first 60 min, although there was no positive postprandial net lipogenesis, and remained <1 in the lean men, as found in other studies (13, 14). This information indicates that there was no net gain in body fat after the administration of a large carbohydrate load.
Using tracer techniques, several authors assessed the effect of carbohydrate on DNL both in isoenergetic diets (10, 15, 18) and during surplus-carbohydrate diets (15, 33) and reported that carbohydrate consumption produced a dose-dependent increase in fractional DNL. Nevertheless, it remained unimportant to body fat stores because it represented only a few grams per day, when the absolute rate of lipogenesis was measured.
This study's aim was to see if this occurred in overweight men as well. These men had elevated fasting levels of glucose, insulin, triglycerides and DNL rate. The overweight men responded differently to the high carb meal with higher DNL, lower fatty acid oxidation rates, increased trigs and NEFA.
Taken together, these results - ... - all point to an impairment of tissue fuel selection (utilization of fatty acids) in the overweight group, in whom a carbohydrate load produced a fat-sparing effect more pronounced than in lean men and so a less negative fat balance than in lean men.
The authors point to a TEF of the carbohydrate load in the overweight men which goes counter to the LC dogma. This could not be correlated to the energy cost of DNL b/c that was not measured.
But here's some "red meat" for the carbs turn to fat crowd:
... the fact remains that obesity can develop from overeating simple carbohydrates, especially in persons who show a higher hepatic fat synthesis and lower fat oxidation during carbohydrate overfeeding.Taubesians will read that and ignore the rest of this study, however. The discussion goes on to say:
Because the heavier participants in this study were already overweight, it is uncertain whether these responses to carbohydrate intake contribute to the development of obesity, but it clearly could contribute to the maintenance of their overweight state.
The fatty acids and triglycerides created through DNL go into various lipid "pools" in the body. Once there, they are indistinguishable from lipids from other sources, namely diet and adipose tissues. In lean men, the excess carbs were not converted to fats in any significant manner. The hierarchy of fuel usage -- where fats are the last on the list -- has been pretty well established, and as the study authors implied, their fuel selection process is in "good repair". I don't get excited by the whole carbs suppress fat burning thing because they will only do so until you run out of them. The fact is that DNL occurs in the fasted state. The fact is that DNL also occurs at fairly low rates in all cases so it is somewhat alarmist to point to 2 or 3 fold increases (temporarily) in the rate. The fats created through this process are metabolically equivalent to ingested fats that are continually undergoing slow turnover in our fat cells. They are a few drops in the pool and will be "burned" in due time when energy requirements dictate. They will only add (net) to STORED fats if there's a chronic positive energy balance. If anything, the "genesis" of lipids from carbs requires some energy. All of this does not address whether some may overeat carbs, and certainly refined carby foods make this really easy to do. I continue to contend that for most, however, this overeating is of foods rich in carbs and fat. However, once someone is obese, I believe LC induces a metabolic state that can and should more easily allow the person to lose weight -- e.g. return to a normal metabolic state. Absent permanent damage (e.g. impaired ß-cells) I believe one can return to a "lean metabolism" and handle carbs once the "overstuffed" state has been ameliorated.