DIETARY INULIN LOWERS PLASMA-CHOLESTEROL AND TRIACYLGLYCEROL AND ALTERS BILIARY BILE-ACID PROFILE IN HAMSTER

Citation
Ea. Trautwein et al., DIETARY INULIN LOWERS PLASMA-CHOLESTEROL AND TRIACYLGLYCEROL AND ALTERS BILIARY BILE-ACID PROFILE IN HAMSTER, The Journal of nutrition, 128(11), 1998, pp. 1937-1943
Citations number
36
Categorie Soggetti
Nutrition & Dietetics
Journal title
ISSN journal
00223166
Volume
128
Issue
11
Year of publication
1998
Pages
1937 - 1943
Database
ISI
SICI code
0022-3166(1998)128:11<1937:DILPAT>2.0.ZU;2-6
Abstract
The mechanisms by which inulin may elicit its lipid-lowering effect ar e not well elucidated. To examine the lipid-lowering potential of inul in and especially its effect on bile acid metabolism, male golden Syri an hamsters were fed semipurified diets containing 20 g/100 g fat, 0.1 2 g/100 g cholesterol and 0 (control), 8, 12 or 16% inulin for 5 wk. P lasma total cholesterol concentrations were significantly lowered by 1 8, 15 and 29% in hamsters fed 8, 12 and 16% inulin, respectively. Diet ary inulin specifically decreased VLDL cholesterol, which was signific antly lower in hamsters fed 16% inulin compared with controls (1.1 +/- 0.3 vs. 2.9 +/- 0.6 mmol/L). LDL and HDL cholesterol were not signifi cantly affected by dietary inulin. Plasma triacylglycerol was signific antly reduced by 40 and 63% in hamsters fed 12 and 16% inulin, respect ively. Hepatic total cholesterol and particularly esterified cholester ol accumulation were significantly lower in hamsters fed 8% inulin com pared with controls. All three levels of dietary inulin caused distinc t alterations in the bile acid profile of gallbladder bile. Taurocheno deoxycholic acid was significantly lower, whereas glycocholic and glyc odeoxycholic acid were greater in hamsters fed inulin. Daily fecal bil e acid excretion (mu mol/d) tended to be greater (P = 0.056) in inulin -fed hamsters compared with controls, whereas daily neutral sterol exc retion was not affected. These data demonstrate that the lipid-lowerin g action of inulin is possibly due to several mechanisms, including al tered hepatic triacylglycerol synthesis and VLDL secretion and impaire d reabsorption of circulating bile acids.