Low levels of viscous hydrocolloids lower plasma cholesterol in rats primarily by impairing cholesterol absorption

Citation
Ma. Levrat-verny et al., Low levels of viscous hydrocolloids lower plasma cholesterol in rats primarily by impairing cholesterol absorption, J NUTR, 130(2), 2000, pp. 243-248
Citations number
47
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
130
Issue
2
Year of publication
2000
Pages
243 - 248
Database
ISI
SICI code
0022-3166(200002)130:2<243:LLOVHL>2.0.ZU;2-7
Abstract
Hydrocolloids have been proposed as cholesterol-lowering agents, but their viscosity limits their use in human nutrition. A low level (1%) of hydrocol loids (guar gum, (GG); xanthan gum, (XG); and konjac mannan) was investigat ed in rats fed 0.2 g/100 g cholesterol diets. Food intake and body weight g ain were not altered by the diets. Bile flow and cholesterol bile flux were not modified by diet, whereas the bile acid flux was greater in rats fed h ydrocolloid diets. The cecal pool of bile acids was greater than control ra ts only in rats fed the XG diet (+71%, P < 0.001). The fecal excretion of n eutral sterols was stimulated in rats fed the hydrocolloid diets; cholester ol apparent digestibility (60% in controls) was reduced to 30-36% in rats f ed hydrocolloids. Bile acid fecal excretion was not altered by diet treatme nt. As a result, apparent steroid balance was about +40 mu mol/d in control s and only +10 to +20 mu mol/d in rats fed hydrocolloids. Both plasma chole sterol and triglycerides were significantly lower than controls in rats fed XG, but only cholesterol was lower in rats fed the GG diet. These effects were essentially found in the d < 1.040 kg/L fraction. Liver cholesterol co ntent was significantly lower than in controls in rats fed the GG or XG die ts. Liver HMG CoA reductase was not affected by the hydrocolloid diets. In conclusion, a low percentage of viscous hydrocolloids lowers plasma cholest erol in cholesterol-fed rats. Inhibition of intestinal cholesterol absorpti on may be the primary mechanism.