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SCFA which is reflected in higher epithelial and portal concentrations. SCFA concentration in the periphery, however, is very low and therefore difficult to measure accurately so any increase in production of SCFA in response to RS consumption may not be detectable in the peripheral circulation. emic and/or insulinemic responses to RS ingestion. In general, it is accepted that RS consumption lowers post- prandial glucose concentrations marginally and postpran- dial insulin concentrations markedly. Many groups report a decrease in postprandial glycemic or insulinemic responses to RS ingestion relative to digestible starch (DS) consumption [2-7], whereas some report no change [8- 11]. It is important to note that the fat content of the diet has a significant impact on the glycemic response to a meal and some meal tests contained no fat or the fat con- tent of the meal varied among the different RS diets mak- ing results from these studies difficult to interpret [2-4]. Also, there are many sources of RS, such as beans, high amylose corn starch, and potatoes, which possess differ- ent physicochemical properties. So, the source of RS can influence the glycemic/insulinemic response to RS ingestion. ingestion and postprandial metabolite and hormone con- centrations. Fewer studies have documented the effect of RS on lipid metabolism. In humans, five weeks of RS feed- ing lowered fasting cholesterol and triglyceride concentra- tions and postprandial plasma insulin concentrations relative to digestible starch (DS) feeding [12,13]. It has also been reported that chronic RS feeding in rats causes a decrease in adipocyte cell size relative to DS feeding [14,15]. In addition, expression of fatty acid synthase was lower in rats fed a RS-based diet than in those fed a DS- based diet [16]. Taken together, these studies provide evi- dence that RS intake has an effect upon the activity of key lipogenic enzymes and adipocyte morphology. Thus, it seems that the effects of this carbohydrate subtype on lipid metabolism should be carefully examined in human studies. and dietary lipid may slow the absorption, and thereby increase the oxidation, of dietary lipid. Currently, there is no evidence pertaining to the dose-response relationship for RS ingestion (as part of a mixed meal) and postpran- dial glycemia, insulinemia, fat oxidation, or meal fat stor- age. It is important that these parameters be defined before designing and conducting long-term, prospective RS feeding studies. FFA, or triglyceride concentration was observed between any of the RS doses examined (Figure 1). ence on RQ (respiratory quotient) values (F-test, 0.04; Figure 2). This overall effect was due to a significantly lower RQ at the 5.4% RS dose than the 0% (p = 0.02) or 10.7% (p = 0.009) RS doses, indicating an increase in fat oxidation in response to the 5.4% RS meal relative to the 0% and 10.7% RS doses (Figure 2). RQ was significantly lower for the 5.4% RS meal than 0% RS meal at 120, 240, 300 and 360 minutes (p = 0.05, 0.03, 0.02 and 0.04, respectively) whereas significant differences occurred at 120, 180, 240, 300 and 360 minutes (p = 0.01, 0.01, 0.005, 0.02, and 0.03, respectively) for the 5.4% RS versus 10.7% RS meals. These data are reflected in total macro- nutrient oxidation rates (Figure 3), which show a signifi- cant increase in the amount of fat oxidized at the 5.4% RS dose relative to the 0% RS meal, with a concomitant decrease in total carbohydrate oxidation. tion at the 5.4% RS dose was significantly higher than both the 0% (p = 0.0062) and 10.7% doses (p < 0.0001). Separate tests at 6 h or 24 h following the test meal gave comparable results (Figure 4a). Taken together, these independent measurements of fat oxidation (indirect calorimetry, oxidation of [ prandial fat oxidation. Unexpectedly, this effect was lost if the dose was increased to 10.7% RS. assessed by incorporation of although this effect did not reach statistical significance (Figure 4b). mixed meal, balanced for total fat and fiber content, had no effect on postprandial glucose, insulin, FFA, or triglyc- eride excursions. However, meals containing a moderate amount of RS caused an increase in fat oxidation as meas- ured by both indirect calorimetry and the production of and fat oxidation was not linear. Although this result is difficult to explain in the current context, it emphasizes the need for careful selection of RS dose in prospective feeding studies. |
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