We investigated the potential beneficial effects of Bifidobacterium animalis on intestinal damage using zinc-deficient (ZD) rats as a model for intestinal alterations. The ZD rats were fed diets containing 1 mg Zn/kg for 20 (ZD20) or 40 (ZD40) d to induce damage that differed in severity. Subgroups of these rats, the ZD20 + B and ZD40 + B groups, received a suspension of B. animalis (3.5 x 108 colony forming units) daily for the last 10 d. Another subgroup, the ZD40 + B + 7 d group, was fed the ZD diet for 7 d after the B. animalis treatment period. Zinc deficiency induced ulcerations, edema, inflammatory cell infiltration and dilatation of blood vessels in duodenum, jejunum and ileum, with increasing severity between 20 and 40 d of zinc deficiency. The mucosa of the ZD20 + B group was well preserved, and most of the morphologic alterations induced by zinc deficiency were normalized in the ZD40 + B group. The high fecal concentrations of B. animalis in the ZD40 + B and ZD40 + B + 7 d groups indicate that these bifidobacteria survived passage through the gastrointestinal tract and proliferated. Electron microscopy confirmed the elevated numbers of bifidobacteria in cecum. Treatment with B. animalis resulted in greater epithelial cell proliferation and disaccharidase activities in the ZD40 + B group compared with the ZD40 group. These findings indicate that B. animalis can protect the intestine from alterations induced by zinc deficiency, suggesting that this bacterium may play a role in intestinal mucosal defense.

Bifidobacterium animalis protects intestine from damage induced by zinc deficiency in rats

Brandi G.;Biavati B.
1999

Abstract

We investigated the potential beneficial effects of Bifidobacterium animalis on intestinal damage using zinc-deficient (ZD) rats as a model for intestinal alterations. The ZD rats were fed diets containing 1 mg Zn/kg for 20 (ZD20) or 40 (ZD40) d to induce damage that differed in severity. Subgroups of these rats, the ZD20 + B and ZD40 + B groups, received a suspension of B. animalis (3.5 x 108 colony forming units) daily for the last 10 d. Another subgroup, the ZD40 + B + 7 d group, was fed the ZD diet for 7 d after the B. animalis treatment period. Zinc deficiency induced ulcerations, edema, inflammatory cell infiltration and dilatation of blood vessels in duodenum, jejunum and ileum, with increasing severity between 20 and 40 d of zinc deficiency. The mucosa of the ZD20 + B group was well preserved, and most of the morphologic alterations induced by zinc deficiency were normalized in the ZD40 + B group. The high fecal concentrations of B. animalis in the ZD40 + B and ZD40 + B + 7 d groups indicate that these bifidobacteria survived passage through the gastrointestinal tract and proliferated. Electron microscopy confirmed the elevated numbers of bifidobacteria in cecum. Treatment with B. animalis resulted in greater epithelial cell proliferation and disaccharidase activities in the ZD40 + B group compared with the ZD40 group. These findings indicate that B. animalis can protect the intestine from alterations induced by zinc deficiency, suggesting that this bacterium may play a role in intestinal mucosal defense.
JOURNAL OF NUTRITION
Mengheri E.; Nobili F.; Vignolini F.; Pesenti M.; Brandi G.; Biavati B.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11585/875716
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