SummaryThis study was conducted to know the possibility that pectin-induced alterations in lipid metabolism of animals might be partly ascribed to galacturonic acid produced by the degradation of ingested pectin in the digestive tract. After a 4-week meal feeding twice a day, fasted rats were fed glucose and fructose and 3h later orally administered 213mg of pectin (from apple) or galacturonic acid per kg of body weight, or fed water alone. Significant changes in serum and liver lipids were observed 30min and 1h after the administration of pectin and galactu ronic acid but not 5h after the administration. Pectin and galacturonic acid showed contradictory effects on serum lipids, adipose tissue lipo protein lipase activity and triacylglycerol (TG) production and removal rates. However, the elevation of total lipid and TG levels in liver with the sugar feeding was significantly inhibited by the administration of either pectin or galacturonic acid. These results support our hypothesis that galacturonic acid produced by the degradation of ingested pectin in the digestive tract may be partly responsible for the pectin-induced changes in lipid metabolism. This was discussed in relation to another possible regulation of lipid metabolism by short-chain fatty acids which are produced by the intestinal fermentation of pectin and galacturonic acid.
SummaryThe present study was undertaken to determine whether the timing of sucrose meal feeding relative to periods of physical activity affects plasma triacylglycerol (TG) levels in rats. Animals were daily meal fed on a basal diet and a 35% sucrose diet for 10 weeks. Meal times were at 08.00-09.00 hr and 21.00-22.00hr. Voluntary running in wheels was allowed between 22.00-08.00hr, but was restricted from 08.00 to 22.00hr. The sucrose diet was given at the morning meal time to one group (M-S eaters) and at the evening meal time to another group (E-S eaters). The timing of the sucrose meal did not have any influence on consumption of either of the two diets, physical activity, weight gain, or the weight of several organs and tissues. Plasma TG, however, was significantly higher in the M-S eaters than in the E-S eaters. Lipoprotein lipase activity of several tissues was not affected by the timing of the sucrose meal. The Triton-induced increase in fasting plasma TG was significantly higher after the sucrose meal than after the basal meal regardless of the timing of the sucrose diet. The TG accumulation rate during the physically inactive period was significantly greater in the M-S eaters than in the E-S eaters, while during the physically active period it was equal in both groups. These results suggest that the effect of sucrose feeding on plasma TG may be conditioned by the timing of sucrose feeding and rats' physical activity.
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