An energy-rich diet causes rumen papillae proliferation associated with more IGF type 1 receptors and increased plasma IGF-1 concentrations in young goats
An energy-rich diet causes rumen papillae proliferation associated with more IGF type 1 receptors and increased plasma IGF-1 concentrations in young goats
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DOI:
10.1093/jn/134.1.11
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发表时间:
2004-01-01
影响因子:
4.2
通讯作者:
Voigt, J
中科院分区:
文献类型:
--
作者:
Shen, ZM;Seyfert, HM;Voigt, J
We tested the hypothesis that the dietary energy-dependent alterations of the rumen papillae size are accompanied by corresponding changes in systemic insulin-like growth factor (IGF)-1 concentration and in rumen papillary IGF type 1 receptors (IGF-1R). Young male goats (n = 24) were randomly allocated to two groups (n = 12) and fed a high level (HL) metabolizable energy [1200 kJ/(kg(0.75.)d)] or a low level (LL) [500 kJ/(kg(0.75.)d)] diet for 42 d. The concentration of ruminal total SCFA did not differ between the groups, but the molar proportion of butyric acid was enhanced by 70% in the HL group (P < 0.05). Both the length and width of the papillae were greater (P < 0.05) in the HL group, and the surface was 50-100% larger (P < 0.05) in the tissue sampled from the artrium ruminis, the ventral ruminal sac and the ventral blind sac. Transport of Na+ across the rumen epithelium, which is amiloride sensitive, was higher (P < 0.05) in the HL than in the LL group. Furthermore, the plasma IGF-1 concentration was about twofold higher in the HL group (P < 0.05), and the maximal rumen epithelial IGF-1 R binding was also higher in the HL (P < 0.05) than in the LL group. IGF-1 R mRNA and IGF-1 mRNA were detected in rumen papillae; however, they were unaffected by dietary treatments. DNA synthesis and cell proliferation of cultured rumen epithelial cells were higher (P < 0.05) after IGF-1 treatment (25 or 50 mug/L) compared with those in the medium without IGF-1. Thus dietary energy-dependent alterations of rumen morphology and function are accompanied by corresponding changes in systemic lGF-1 and ruminal lGF-1R.