A feeding study was performed to investigate possible performance enhancing effects of rare earth elements (REE) in growing and fattening pigs, as well as their influence on the blood serum biochemical changes and the accumulation of REE in the organs of pigs treated with a REE diet for a longer time period. Fourteen crossbred piglets (Deutsche Landrasse x Piétrain) were allotted to two dietary treatments: a control group and the REE-treated group which was supplemented with 300 mg of an REE mixture per kg feed. The REE mixture contained mainly chlorides of lanthanum (La), cerium (Ce) and praseodymium (Pr). The whole feeding period consisted of a 2 months ad libitum feeding period M-I and a 1 month restricted feeding period M-II. It was found that in comparison with the control group, the REE group had a better daily body weight gain of 19% (p < 0.05) in the period M-I and 12% in the period M-II; the REE group also had a better feed conversion ratio of 11% in period M-I and 3% (p > 0.05) in the period M-II. The REE had no significant (p > 0.05) influence on blood serum thyroxine (T(4)), aspartate-amino-transferase (AST), alanine-amino-transferase (ALT), alkaline-phosphatase (AP), total cholesterol, triglyceride, total protein, albumin, glucose, Ca, P, Na, K and Cl. However, serum triiodothyronine (T(3)) in the REE group was significantly (p < 0.01) lower than that in the control group. The accumulation rate of La and Ce in the muscle, liver and kidneys was very low after feeding the REE diet for 3 months. The study indicates the possibility of using rare earth elements as safe and inexpensive alternative performance enhancers for pig production.

Insulin-like growth factor-binding protein-2 (IGFBP-2) has been suggested to be a negative regulator of bone growth and maintenance. The objective of this study was to characterize the effect of elevated IGFBP-2 on the skeletal phenotype of adult transgenic mice, in the absence and presence of growth hormone (GH) excess. 43 male mice were examined at an age of 4 months (7 IGFBP-2 transgenic mice, 12 GH transgenic mice, 10 mice carrying both transgenes, and 14 controls). The bone mineral content of the total skeleton and of isolated bones was quantified by dual energy X-ray absorptiometry (DXA), after validation versus ash analysis. Cortical and trabecular bone was quantified by peripheral quantitative computed tomography (pQCT), after validation versus microCT. A strong linear relationship was found between DXA and ash weight, and between pQCT and micro CT ( r>0.95). Bone size and bone mineral content were significantly reduced in IGFBP-2 transgenic mice, the magnitude of the effect varying between skeletal sites and between bone compartments. Elevated IGFBP-2 negatively modulated the GH-stimulated increase in bone size and mineral content, and completely blocked GH-effects at cortical sites. Notably, bone density was not decreased in IGFBP-2 transgenic animals compared with controls. In conclusion, IGFBP-2 is identified as a potent negative regulator of normal and GH-stimulated bone growth in vivo. Interestingly, elevated IGFBP-2 levels did not lead to a decrease in bone density, suggesting that IGFBP-2 negatively affects bone size and mineral content, but not bone maintenance in adult mice.

The objective of this study was to directly compare in situ femoral dual-energy X-ray absorptiometry (DXA) and in vitro chemical analysis (ash weight and calcium) with mechanical failure loads of the proximal femur, and to determine the influence of bone size (volume) and density on mechanical failure and DXA-derived areal bone mineral density (BMD, in g/cm2). We performed femoral DXA in 52 fixed cadavers (age 82.1 +/- 9.7 years; 30 male, 22 female) with intact skin and soft tissues. The femora were then excised, mechanically loaded to failure in a stance phase configuration, their volume measured with a water displacement method (proximal neck to lesser trochanter), and the ash weight and calcium content of this region determined by chemical analysis. The correlation coefficient between the bone mineral content (measured in situ with DXA) and the ash weight was r = 0.87 (standard error of the estimate = 16%), the ash weight allowing for a better prediction of femoral failure loads (r = 0.78; p < 0.01) than DXA (r = 0.67; p < 0.01). The femoral volume (r = 0.61; p < 0.01), but not the volumetric bone density (r = 0.26), was significantly associated with the failure load. The femoral bone volume had a significant impact (r = 0.35; p < 0.01) on the areal BMD (DXA), and only 63% of the variability of bone volume could be predicted (based on the basis of body height, weight and femoral projectional bone area. The results suggest that accuracy errors of femoral DXA limit the prediction of mechanical failure loads, and that the influence of bone size on areal BMD cannot be fully corrected by accounting for body height, weight and projected femoral area.

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