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(Journal of Nutrition. 1999;129:1467S-1470S.)
© 1999 The American Society for Nutritional Sciences

Supplement

Biochemical Basis of Oligofructose-Induced Hypolipidemia in Animal Models1

Nathalie M. Delzenne2 and Nadine N. Kok

Unité de Biochimie Toxicologique et Cancérologique, Université Catholique de Louvain, UCL-PMNT 7369-B-1200 Brussels, Belgium

2To whom correspondence should be addressed.

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.

KEY WORDS: • fructan • triglycerides • lipogenesis • rat • liver • oligofructose






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