Effect of nondigestible oligosaccharides on glucose and lipid metabolism a phenomenon linked to a decrease in food intake

7.4.1 Non-digestible oligosaccharides and lipid/glucose metabolism in animal studies

Most data published to date relate to experimental studies performed in animals. NDOs are able to modulate hepatic lipid metabolism in rats or hamsters, with consequences on either triglyceride accumulation in the liver, and/or serum lipids. In non-obese rats and/or hamsters fed a high-

carbohydrate diet, a decrease in hepatic and serum triglycerides is observed when inulin-type FOS are added to the diet at concentrations from 2.5 to 10% for several weeks (from 2 to 12 weeks) (Delzenne & Williams 2002). In animals, reduced triglyceridaemia is often linked to a decrease in de novo lipogenesis in hepatic, but not in adipose, tissue, cells. A decrease in the expression of key hepatic lipogenic enzymes, reflected by a decrease in fatty acid synthase mRNA, seems to be involved in the lower lipogenic capacity after inulin-type FOG supplementation, as also shown with resistant starch (Delzenne et al. 2002). In rats fed a lipid-rich diet containing 10% FOS, a decrease in triglyceridaemia also occurs without any protective effect on hepatic triglyceride accumulation and lipogenesis, suggesting a possible peripheral mode of action (Kok et al. 1998b). By contrast, in obese Zucker rats, dietary supplementation with FOS lessens hepatic steatosis, with no effect on post-prandial triglyceridaemia when added in the standard diet (Daubioul et al. 2000). This effect is likely to result mainly from reduced availability of non-esterified fatty acids coming from adipose tissue, since fat mass and body weight are decreased by the treatment. The protection against steatosis is strongly dependent on fermentation pattern (Daubioul et al. 2002). The high proportion of propionate produced in the caecum, which reaches the liver through the portal vein, is, at least in animals, a key event explaining a lower hepatic triglyceride synthesis upon NDO feeding (Morand et al. 1993; Delzenne et al. 2002; M. Lasa, June 2002, unpublished results).

Rats fed with NDOs (OFS), also exhibit lower fat mass development, as shown in several models (Daubioul et al. 2002; Delzenne et al. 2005). The epididymal, inguinal and visceral adipose tissue fat mass are lowered by 30% to 40% in OFS-fed rats as compared with controls (Cani et al. 2004).

The effects of NDOs on glucose homeostasis have been less well studied. An improvement of glucose/insulin ratio has been observed in rats receiving FOS with a high-fructose diet (Busserolles et al. 2003).

We have recently reported that OFS improves glycaemia and plasma insulin, both in the post-prandial state and after an oral glucose load in streptozotocin-treated diabetic rats (STZ). Moreover, treatment with OFS improves pancreatic insulin and P-cell mass (Cani et al. 2005a). This 'antidiabetic' effect of NDOs is partly linked to a decrease in food intake due to the treatment, but is merely due to the promotion of incretins production (see 7.6.2). In diabetes prone-BB rats, which are characterised by a default in the production of gut peptides, no effect of OFS was shown (Perrin et al. 2003)

In most studies showing the interesting effects of NDOs on lipid or glucose metabolism, and fat mass development, the animals supplemented with NDOs exhibited a lower energy intake, suggesting that NDOs have a satietogenic effect. How does this take place? Is it really one of the important metabolic effects of NDOs? The second part of the chapter will be devoted to these questions.

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