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tate:butyrate:propionate ratio compared to fermentation of non-starch polysaccharides [29]. In particular, the amount of butyrate is substantially elevated in response to RS fermentation [30,31]. In humans fed a low or high RS diet for three days, the concentration of excreted SCFA rose from 20 mmol/d to 33 mmol/d, respectively [19]. This increase in total SCFA concentration was caused by a doubling of the acetate and butyrate content changing the acetate:butyrate:propionate ratio from 12:3:3 to 21:6:4 in response to the low and high RS diets, respectively. ing evidence for the role of SCFAs in carbohydrate and lipid metabolism [26,32-34]. Acetate and/or butyrate have been shown to decrease glycogenolysis and glycoly- sis in isolated rat and sheep hepatocytes [35-37]. So, it is plausible that the fermentation of RS from the 5.4% RS diet increases the net production of SCFAs which inhibit glycolysis in the liver. In this scenario, the liver, deprived of carbohydrate-derived acetyl CoA would be more reliant on fat-derived acetyl CoA as a fuel source, thereby contrib- uting to an overall increase in fat oxidation [17]. This pos- sibility needs to be investigated in future studies. maximal 10.7% dose of RS and the 0% dose. This is an unexpected result that is difficult to explain. The loss of any effect on fat oxidation when the RS dose in the meal was increased to 10.7% may occur because this dose is at the threshold of the starch's properties as RS. That is, at the 10.7% dose of RS, the starch may not be completely fer- mented in the large bowel thereby causing a loss of energy from the diet via the feces. If this is the case, the strong physical association between RS and dietary lipid may cause excretion of lipid and therefore, less dietary fat to be available for oxidation at the 10.7% dose. Indeed, it has previously been shown that intake of high-amylose maize starch, such as that used in this study, caused an increased number of bowel actions per day [18]. RS has also been shown to decrease colonic transit time and, as more RS enters the large bowel, more starch is also excreted [19,20]. This indicates that, at higher levels of RS con- sumption, only a portion of the RS can be fermented and the remainder passes through the colon as an insoluble fiber. Furthermore, if indeed RS at the 10.7% dose is being excreted as insoluble fiber, less fermentation and SCFA production would be occurring. As SCFA are hypothesized to be the cause of the observed increase in fat oxidation in Total fat (a) and carbohydrate (b) oxidation in response to RS content of a breakfast meal. Macronutrient oxida- tion, assessed via indirect calorimetry and calculated from non-protein RQ, was measured in 12 healthy adults. Data is pre- sented as mean ± SEM. * p 0.003 for a difference from the 0% and 10.7% RS meals. a at g a oxidat |
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Study 