Low-dietary protein intake induces problems with glucose homeostasis and results in hepatic steatosis in heavy milk-fed calves

被引:9
作者
Gerrits, W. J. J. [1 ]
van den Borne, J. J. G. C. [1 ]
Blum, J. W. [2 ]
机构
[1] Univ Wageningen & Res Ctr, Anim Nutr Grp, NL-6700 AH Wageningen, Netherlands
[2] Univ Bern, Fac Vet, Div Nutr & Physiol, CH-3012 Bern, Switzerland
关键词
veal calves; protein intake; energy intake; insulin resistance; fatty liver;
D O I
10.1016/j.domaniend.2007.10.002
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
We studied effects of protein intake at two protein-free energy intake levels on plasma glucose and insulin concentrations, urinary glucose excretion and on liver and intestinal fat content in milk-fed veal calves. Two experiments were performed at body weights (BW) of 80-160 kg (mean 120 kg; Exp. 1) and 160-240 kg (mean 200 kg; Exp. 2). In each experiment, 36 calves were allocated to one of six protein intake levels, at each of two energy intake levels. Digestible protein intakes ranged between 0.90 and 2.72 g nitrogen (N)/(kg BW (0.75) x d) in Exp. 1 and between 0.54 and 2.22 g N/(kg BW (0.75) x d) in Exp. 2. The two energy intake levels were kept constant on a protein-free basis and were 663 and 851 kJ/(kg BW0.75 x d) in Exp. 1 and 564 and 752 kJ/(kg BW0.75 x d) in Exp. 2. Blood samples were taken between 5 and 6 h post-feeding at 14-d intervals until calves reached target BW, and liver fat mass was determined at slaughter. Urinary glucose excretion was quantified at 120 and 200kg BW in Exps. 1 and 2, respectively. Increased protein-free energy intake increased plasma glucose concentrations and urinary glucose losses in 200 kg calves, but not in 120 kg calves. Increasing protein intake decreased plasma glucose, urinary glucose and plasma insulin in both experiments. Liver fat content decreased with increasing protein intake. In conclusion, long-term low-dietary protein intake increased hyperglycemia, hyperinsulinemia, glucosuria and hepatic steatosis in heavy milk-fed calves, likely associated with increased insulin resistance. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:121 / 129
页数:9
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