BACKGROUND: While naturally occurring inulin has anti-hyperlipidemic effects in animals and humans, health effects of synthetic inulin with different degrees of fructose polymerization remain poorly understood. AIM OF THE STUDY: Our study aimed at distinguishing health effects of synthetic inulin with different degrees of fructose polymerization (DP) from those of resistant maltodextrin and clofibrate. METHODS: We examined effects of synthetic inulin on serum and liver lipid profiles and blood biochemical parameters in rats fed a high-fat and high-sucrose (HF, cafeteria) diet when compared to resistant maltodextrin and clofibrate. RESULTS: Treatment with inulin (average DP = 6-8, 16-17 and 23) and resistant maltodextrin for 3 weeks reduced the elevation in liver levels of triacylglycerol and total cholesterol of rats fed the cafeteria diet but not the standard diet. In these groups, inulin (average DP = 16-17) significantly reduced the portal plasma glucose level. Moreover, the levels of portal plasma propionate and circulating serum adiponectin, which were decreased in cafeteria rats, recovered to nearly normal levels after administration of inulin (average DP = 16-17). In addition, the dietary inulin suppressed elevation in levels of portal plasma insulin and circulating serum leptin and induction of acetyl-CoA carboxylase and fatty acid synthase mRNAs in the liver of cafeteria rats, consistent with the reduction of liver lipids. The dietary inulin and clofibrate markedly reduced triacylglycerol levels in serum very low density lipoprotein (VLDL) and liver and epididymal adipose tissue weights of cafeteria rats; the extent of suppression by the dietary inulin was higher than that by clofibrate. No additive or synergistic effect of the dietary inulin and clofibrate was found in decrease in circulating serum VLDL and liver lipid levels. CONCLUSION: These observations indicate that the dietary inulin may prevent the development of metabolic disease such as hyperlipidemia and hyperinsulinemia caused by intake of cafeteria diet, in association with suppression of liver lipogenesis.
BACKGROUND: While naturally occurring inulin has anti-hyperlipidemic effects in animals and humans, health effects of synthetic inulin with different degrees of fructose polymerization remain poorly understood. AIM OF THE STUDY: Our study aimed at distinguishing health effects of synthetic inulin with different degrees of fructose polymerization (DP) from those of resistant maltodextrin and clofibrate. METHODS: We examined effects of synthetic inulin on serum and liver lipid profiles and blood biochemical parameters in rats fed a high-fat and high-sucrose (HF, cafeteria) diet when compared to resistant maltodextrin and clofibrate. RESULTS: Treatment with inulin (average DP = 6-8, 16-17 and 23) and resistant maltodextrin for 3 weeks reduced the elevation in liver levels of triacylglycerol and total cholesterol of rats fed the cafeteria diet but not the standard diet. In these groups, inulin (average DP = 16-17) significantly reduced the portal plasma glucose level. Moreover, the levels of portal plasma propionate and circulating serum adiponectin, which were decreased in cafeteria rats, recovered to nearly normal levels after administration of inulin (average DP = 16-17). In addition, the dietary inulin suppressed elevation in levels of portal plasma insulin and circulating serum leptin and induction of acetyl-CoA carboxylase and fatty acid synthase mRNAs in the liver of cafeteria rats, consistent with the reduction of liver lipids. The dietary inulin and clofibrate markedly reduced triacylglycerol levels in serum very low density lipoprotein (VLDL) and liver and epididymal adipose tissue weights of cafeteria rats; the extent of suppression by the dietary inulin was higher than that by clofibrate. No additive or synergistic effect of the dietary inulin and clofibrate was found in decrease in circulating serum VLDL and liver lipid levels. CONCLUSION: These observations indicate that the dietary inulin may prevent the development of metabolic disease such as hyperlipidemia and hyperinsulinemia caused by intake of cafeteria diet, in association with suppression of liver lipogenesis.
Authors: Gary James Grover; Lee Koetzner; Joan Wicks; Roland J Gahler; Michael R Lyon; Raylene A Reimer; Simon Wood Journal: Front Pharmacol Date: 2011-09-07 Impact factor: 5.810
Authors: Frederique Respondek; Philippe Gerard; Mathilde Bossis; Laura Boschat; Aurélia Bruneau; Sylvie Rabot; Anne Wagner; Jean-Charles Martin Journal: PLoS One Date: 2013-08-12 Impact factor: 3.240