The present study was aimed at answering the question why feeding rats an oligofructose (OFS) supplemented diet could cause a significant reduction in plasma lipid levels. Daily administration of a 10% (w/w) OFS-containing diet to normolipidemic male rats resulted in a decrease in plasma triglycerides, phospholipids and cholesterol. The triglyceride-lowering effect was observed after one week and lasted for at least 16 wk and was associated with a reduction in plasma very low density lipoproteins, indicating that the hypolipidemic effect of OFS may be due to changes in liver lipid metabolism. We therefore tested whether OFS feeding modified the capacity of the liver to synthesize triglycerides from free fatty acids. Hepatocytes isolated from livers of control and OFS-fed rats were incubated in the presence of [1-14C]palmitate, and both intracellular and extracellular [14C]triglyceride formation were quantified. We found that chronic feeding of an OFS-supplemented diet to rats significantly reduced the capacity of isolated hepatocytes to synthesize triglycerides from palmitate. The results suggest that, like other soluble dietary fibers, OFS significantly alters liver lipid metabolism, resulting over time in a significant reduction in plasma triglyceride, phospholipid and cholesterol levels.

Several nondigestible but fermentable dietary carbohydrates are able to regulate lipemia and triglyceridemia in both humans and animals. The mechanism of their serum lipid-lowering effect remains to be elucidated. Oligofructose, which is a mixture of nondigestible and fermentable fructans, can decrease triacylglycerol in VLDL when given to rats. The triacylglycerol-lowering action of oligofructose is due to a reduction of de novo fatty acid synthesis in the liver through inhibition of all lipogenic enzymes, namely acetyl-CoA carboxylase (EC 6.4.1.2), fatty acid synthase, malic enzyme (EC 1.1.1.40), ATP citrate lyase (EC 4.1.3.8), and glucose-6-phosphate dehydrogenase (EC 1.1.1.49). Our results suggest that oligofructose decreases lipogenic enzyme gene expression. Postprandial insulin and glucose concentrations are low in the serum of oligofructose-fed animals and this could explain, at least partially, the metabolic effect of oligofructose. Moreover, some events occurring in the gastrointestinal tract after oligofructose feeding could be involved in the antilipogenic effect of this fructan: the production of propionate through fermentation, a modulation of the intestinal production of incretins (namely glucose-dependent insulinotropic peptide and glucagon-like peptide-1), or the modification of the availability of digestible carbohydrates. Recent studies showed that the hypotriglyceridemic effect of fructans also occurs in humans.

Dietary supplementation with oligofructose (Om; 100 g/kg), a nodigestible oligomer of /h-fructose, decreases serum triacylglycerols in serum and VLDL of rats. In order to investigate the role of hepatic metabolism in the hypolipidaemic effect of Om, male Wistar rats were fed on a standard diet with or without 1OOg Raftilosee P d k g as OFS source for 30d. OFS feeding (1) significantly decreased triacylglycerol and phqholipid concentrations in both blood and liver, (2) increased the glycerol-3-phosphate liver content but decreased the hepatic activity of glycerol-3-phosphate acyltransferase (EC 2 -3.1. W), suggesting a decrease in acylglycerol synthesis, (3) did not affect the blood non-esterified fatty acid concentrations, but (4) reduced by 54% the capacity of isolated hepatocytes to synthesize and secrete triacylglycerols from labelled acetate; the activity of fatty acid synthase, a key lipogenic enzyme was also significantly decreased. These findings suggest that OFS decreases sennu triacylglycerols by reducing de nova fatty acid synthesis in the liver; the lower insulin level in the serum of OFS-fed rats could explain, at least partly, the metabolic effect induced by such nondigestible carbohydrates. Feeding rats on a diet supplemented with oligofructose (OFS; lWg/kg), a nondigestible but fermentable oligomer of /3-D-fructose obtained by enzymic hydrolysis of chicory (Cichorium intybus) inulin, significantly lowers serum TAG and phospholipid (PL) concentrations (Delzenne et al. 1993). This is exclusively due to a decrease in the concentration of plasma VLDL (Fiordaliso et al. 1995). The hepatic synthesis of VLDL involves the biosynthesis of both lipids and apoproteins, their assembly into nascent VLDL particles, and the secretion of mature VLDL into the circulation (Gibbons, 1990).Since newly-synthesized fatty acids are preferentially channelled into VLDL, the lipogenic activity of the liver is a key factor in hepatic VLDL-TAG output (Gibbons, 1990

The addition of oligofructose as a dietary fiber decreases the serum concentration and the hepatic release of VLDL-triglycerides in rats. Because glucose, insulin, insulin-like growth factor I (IGF-I) and gut peptides [i.e., glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1)]) are factors involved in the metabolic response to nutrients, this paper analyzes their putative role in the hypolipidemic effect of oligofructose. Male Wistar rats were fed a nonpurified diet with or without 10% oligofructose for 30 d. Glucose, insulin, IGF-I and GIP concentrations were measured in the serum of rats after eating. GIP and GLP-1 contents were also assayed in small intestine and cecal extracts, respectively. A glucose tolerance test was performed in food-deprived rats. Serum insulin level was significantly lower in oligofructose-fed rats both after eating and in the glucose tolerance test, whereas glycemia was lower only in the postprandial state. IGF-I serum level did not differ between groups. GIP concentration was significantly higher in the serum of oligofructose-fed rats. The GLP-1 cecal pool was also significantly higher. In this study, we have shown that cecal proliferation induced by oligofructose leads to an increase in GLP-1 concentration. This latter incretin could be involved in the maintenance of glycemia despite a lower insulinemia in the glucose tolerance test in oligofructose-fed rats. We discuss also the role of hormonal changes in the antilipogenic effect of oligofructose.

Oligofructose (OFS), a mixture of nondigestible/fermentable fructooligosaccharides, decreases serum triacylglycerol (TAG) when it is included in the standard, fiber-free or high fat diet of rats. This paper summarizes in vivo and in vitro data to establish a biochemical mechanism underlying the hypolipidemic effect of OFS. When OFS is added to the standard (carbohydrate-rich) diet of rats at the dose of 10 g/100 g, a TAG-lowering action occurs as a consequence of a reduction of de novo liver fatty acid synthesis. The depression in the activity of all lipogenic enzymes and fatty acid synthase mRNA suggests that OFS modifies the gene expression of lipogenic enzymes. Through its modulation of de novo lipogenesis, OFS can protect against liver lipid accumulation induced by providing 10% fructose-enriched water for 48 h. OFS also significantly decreases serum insulin and glucose, which are both known to participate in the nutritional regulation of lipogenesis. It also increases the intestinal production of incretins, namely, glucose-dependent insulinotropic peptide and glucagon-like peptide 1. This latter phenomenon results mainly from promotion of intestinal tissue proliferation by oligofructose fermentation end-products. Collectively, a link likely exists between the modulation of hormone and incretin production by OFS, and its antilipogenic effect.