THE EFFECTS OF DIETARY SUGAR-BEET FIBER AND GUAR GUM ON LIPID-METABOLISM IN WISTAR RATS

Citation
Pd. Overton et al., THE EFFECTS OF DIETARY SUGAR-BEET FIBER AND GUAR GUM ON LIPID-METABOLISM IN WISTAR RATS, British Journal of Nutrition, 72(3), 1994, pp. 385-395
Citations number
36
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00071145
Volume
72
Issue
3
Year of publication
1994
Pages
385 - 395
Database
ISI
SICI code
0007-1145(1994)72:3<385:TEODSF>2.0.ZU;2-5
Abstract
This study investigates the mechanisms of action for the hypocholester olaemic effects of sugar-beet fibre (SBF) and guar gum. Four groups of ten male Wistar rats were fed ad lib. on test diets containing either 100 g SBF or guar/kg, or control diets containing 100 g cellulose or wheat bran/kg for 28 d. Food intake, weight gain and food consumption ratios were unaffected by the diets. Circulating cholesterol and hepat ic cholesterol concentrations were significantly lower in both SBF- an d guar-fed groups compared,vith either cellulose- or bran-fed animals. Circulating triacylglycerol concentrations were significantly lower i n SBF- and guar-fed animals, but total hepatic lipid concentrations an d hepatic and adipose tissue lipogenesis rates were unaffected by the diets. Hepatic cholesterol-7 alpha-hydroxylase (EC 1.14.13.17) activit ies were significantly higher in the guar-fed animals compared with ce llulose or bran control groups. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (EC 1.1.1.88) activities,were unaffected. Circulating bile acid concentrations were significantly Lower in SBF- and guar-fed anim als and faecal bile acid output was significantly higher in the guar-f ed group compared with bran- or cellulose-fed groups. This study suppo rts the hypothesis that guar exerts its hypocholesterolaemic effect vi a intraluminal bile acid binding and loss of cholesterol from increase d faecal bile acid excretion. The mechanism of action for the hypochol esterolaemic effect of SBF is less clear; the results of the present s tudy point to a mechanism involving disruption of the enterohepatic bi le acid circulation, possibly via changes in the rate of absorption of dietary lipid.