Various protocols have been developed to induce hyperlipidemy in experimental animals. These are based on changes in diet composition and include:

• Supplementing the standard diet with cholesterol (0.1-0.2 or 1%) with or without cholic acid (0.1-0.2%)22-24

• Using sucrose or fructose as the major (±50-57.5%), if not the only, carbohydrate source in diet25

• Increasing fat content in diet from the recommended 3-5% up to 10-15% or even more

• Combining two of these approaches.

Supplementing such diets with inulin-type fructans has been used to test for their effects on lipid parameters in hyperlipidemic animals, a recognized model for humans at an increased risk of atherosclerosis.

Diets supplemented with cholesterol (0.1-0.2% or 1%) with or without cholic acid (0.1%) have been reported to induce mild to severe hypercholesterolemia in experimental animals. In a protocol designed to investigate the effect of consumption of unprocessed inulin and inulin baked in bread on the lipid metabolism in rats (male Wistar) made hypercholesterolemic (±2-fold increase in plasma total cholesterol, p < 0.05) by adding 1% cholesterol and 0.1% cholic acid, Vanhoof and Deschrijver reported no effect on plasma triglycerides and plasma cholesterol (total, free, or esterified).18 In the same study, the hypercholesterolemic diet increased all liver lipid parameters (i.e., triglycerides, 3.25D; total, 22D, esterified, 54D and free cholesterol, 1.2D; p < 0.05) but inulin (6% w/w in diet) had no effect on any of these parameters.18 Using male Sprague-Dawley rats fed a diet supplemented with 0.2% cholesterol, Kim and Shin similarly reported that feeding a diet supplemented with inulin (5% w/w) had no effect on serum total cholesterol and triglycerides but significantly reduced LDL-cholesterol (28%) while increasing HDL cholesterol (1.12H), thus increasing the ratio of HDL cholesterol over LDL cholesterol (1.43-fold).26 Moreover, the inulin treatment significantly reduced the liver TAGs (47%), but it had no effect on liver PLPs or liver cholesterol. A dried water chicory extract (1 and 5% w/w in diet) had essentially the same effect as inulin.26 In male Syrian hamsters fed a standard diet supplemented with 1% cholesterol without cholic acid, Trautwein et al. reported that inulin (the high molecular weight HP product) significantly reduced the plasma concentration of TAGs and total cholesterol.27 These results show a dose-dependent effect of inulin on plasma TAGs (34, 40, 64% at 8, 12, 16% w/w in diet, respectively) but not on plasma total cholesterol (20, 17, 40% at 8, 12, 16% w/w in diet, respectively). Changes in the concentration of TAGs in the VLDL fraction accounted for most of the decrease in plasma concentration. Regarding total cholesterol, its concentration in VLDL was significantly reduced (62%) only in hamsters receiving the highest dose (16% w/w in diet).27 When the core/surface was calculated (as described above) no apparent difference was found, suggesting no difference in particle size, thus confirming the observation of Fiordaliso et al. in rats.14

High sucrose/fructose diets are hyperlipidemic, especially hypertriglyceri-demic. In male Wistar rats given access to either drinking water containing 10% fructose for 48 h15 or a diet in which fructose was the sole source of carbohydrates for 4 weeks16 an increase in serum triglycerides (1.2D and 2.1D, respectively) has been reported but no effect on total serum cholesterol and PLPs. Adding oligofructose to the diet (10% w/w) to pretreat the rats (30 d) before giving them access to fructose in drinking water did not affect serum PLPs and cholesterol, but it significantly further increased triglyceridemia (1.2D).15 In such a protocol, fructose, oligofructose, or a combination of both had no effect on plasma free fatty acids. In the liver of fructose-fed rats, the concentration of triglycerides was increased

(1.250) but not that of PLPs or cholesterol as compared to control conditions. Prefeeding rats with oligofructose (10% in diet for 30 d) prevented the rise in the hepatic concentration of triglycerides that remained at the control level.15 In a protocol in which male Wistar rats were fed a fructose-rich (65% w/w) diet supplemented with oligofructose (10% w/w) for 4 weeks, the concentration of plasma TAGs was still higher than in rats fed a starch-containing diet (1.7D) but it was lower (33%) than in rats fed a fructose-rich diet without oligofructose. Similar modifications of the concentration of TAGs were observed in the liver, i.e., an increase (1.7D) due to fructose intake both in the presence and in the absence of oligofructose, but also a smaller increase due to fructose intake in the oligofructose-containing/fructose-rich diet as compared to the oligofructose-free/fructose rich diet.16

In Sprague-Dawley rats, a sucrose-rich diet (57.5% w/w) has also been shown to induce hypertriglyceridemia and hyperinsulinemia followed, a few days later, by insulin resistance.27 In male Sprague-Dawley rats, feeding a high sucrose (57.5% w/w) diet increased the concentration of plasma triglycerides (1.9D). Adding oligofructose (10% w/w) to the diet significantly reduced plasma TAGs (30%) and plasma free acids (23%) but had no effect on plasma PLPs, and total and free cholesterol.19

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