GUAR-GUM EFFECTS ON PLASMA LOW-DENSITY-LIPOPROTEIN AND HEPATIC CHOLESTEROL-METABOLISM IN GUINEA-PIGS FED LOW-CHOLESTEROL AND HIGH-CHOLESTEROL DIETS - A DOSE-RESPONSE STUDY

Citation
Ml. Fernandez et al., GUAR-GUM EFFECTS ON PLASMA LOW-DENSITY-LIPOPROTEIN AND HEPATIC CHOLESTEROL-METABOLISM IN GUINEA-PIGS FED LOW-CHOLESTEROL AND HIGH-CHOLESTEROL DIETS - A DOSE-RESPONSE STUDY, The American journal of clinical nutrition, 61(1), 1995, pp. 127-134
Citations number
36
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00029165
Volume
61
Issue
1
Year of publication
1995
Pages
127 - 134
Database
ISI
SICI code
0002-9165(1995)61:1<127:GEOPLA>2.0.ZU;2-A
Abstract
Guinea pigs were fed semipurified diets containing either 0% or 12.5% guar gum (GG) with 0.04% cholesterol or increasing concentrations of G G (0%, 2.5%, 5%, 7.5%, 10%, and 12.5%) with 0.25% cholesterol (by wt). Compared to the 0% GG diet with 0.04% cholesterol, intake of the 12.5 % GG diet with 0.04% cholesterol lowered plasma low-density-lipoprotei n (LDL) concentrations, the ratio of LDL cholesteryl ester to protein, hepatic cholesterol concentrations, and the activity of acyl-CoA:chol esterol acyltransferase (ACAT), and increased 3-hydroxy-3-methylglutar yl coenzyme A (HMG CoA) reductase activity and hepatic apo B/E recepto r number (P < 0.01). Intake of GG by animals fed 0.25% cholesterol die ts resulted in modest effects on hepatic cholesterol pools and plasma LDL concentrations; however, significant negative correlations were fo und between both plasma LDL cholesterol and hepatic free cholesterol c oncentrations with the amount of dietary GG (P < 0.05). Hepatic HMG-Co A reductase was suppressed by the 0.25% cholesterol intake, and GG did not reverse this suppression. In contrast, ACAT activity was negative ly correlated with the amount of dietary GG (P < 0.05), and GG intake increased the number of hepatic apo B/E receptors at all intakes with the 0.25% cholesterol diets. These results demonstrate that intake of GG significantly alters endogenous cholesterol metabolism by decreasin g hepatic cholesterol pools, altering hepatic cholesterol homeostasis, and reducing plasma LDL concentrations.