Reversion by taurine but not by glycine of ovarian hormone deficiency - Induced hypercholesterolemia in aged rats is associated with increased fecal bile acids

Citation
T. Kishida et al., Reversion by taurine but not by glycine of ovarian hormone deficiency - Induced hypercholesterolemia in aged rats is associated with increased fecal bile acids, NUTR RES, 20(12), 2000, pp. 1761-1769
Citations number
34
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
NUTRITION RESEARCH
ISSN journal
02715317 → ACNP
Volume
20
Issue
12
Year of publication
2000
Pages
1761 - 1769
Database
ISI
SICI code
0271-5317(200012)20:12<1761:RBTBNB>2.0.ZU;2-C
Abstract
The effect of taurine and glycine on the ovarian hormone deficiency-associa ted increase in plasma cholesterol concentration were studied in ovariectom ized (ovx) 10-month-old retired breeder female rats. Rats was randomly assi gned to four treatment groups: sham-operated+a casein-based cholesterol-fre e diet (C-diet, sham-C); ovx+C diet (ovx-C); ovx+C diet supplemented by tau rine (50 g/kg diet, ovx-T); and ovx+C diet supplemented with glycine (50 g/ kg diet, ovx-G). Rats were fed these diets for 28 d and killed at midnight in a fed state. Plasma and liver cholesterol concentrations in ovx-C were s ignificantly higher than in sham-C. Bile flow, biliary bile acid secretion and fecal bile acid excretion were not significantly different between sham -C and ovx-C. Plasma cholesterol concentrations in ovx-T and ovx-G were sig nificantly lower than those in ovx-C. Liver cholesterol concentration in ov x-G was significantly higher than in ovx-C but not in ovx-T. Cholesterol 7a -hydroxylase, bile flow, biliary bile acid secretion and fecal bile acid ex cretion in ovx-T were significantly higher than in ovx-C, but not in ovx-G. These results indicate that in the case of taurine but not glycine, increa sed fecal bile acid excretion is one of the factors in the prevention of th e ovarian hormone deficiency-associated increase in plasma cholesterol conc entration. (C) 2000 Elsevier Science Inc.