Ruminants can recycle nitrogen (N) and phosphorus (P), which are essential for vital body processes. Reduced N- and P-intake in ruminants is desirable for economic and ecologic reasons. Simultaneous modulation of mineral homoeostasis and bone metabolism occurs in young goats. This study aimed to investigate potential effects of dietary N- and/or P-restriction on molecular changes in bone metabolism. The twenty-eight young male goats were fed a control diet, an N-reduced diet, a P-reduced diet or a combined N- and P-reduced diet for 6–8 weeks. The N-restricted goats had lower plasma Ca concentration and higher plasma osteocalcin (OC) and CrossLaps concentrations. The P-restricted goats had reduced plasma inorganic phosphate (Pi) concentrations and increased plasma Ca concentrations. Due to the initiation of a signalling pathway that inhibits the fibroblast growth factor 23 (FGF23) expression, this was lower with P-restriction. Consequently, lower Pi concentrations were the main factor influencing the reduction in FGF23. The changes in mineral homoeostasis associated with P-restriction led to a reduction in OC, bone mineral content and mineral density. Simultaneously, bone resorption potentially increased with P-restriction as indicated by an increased receptor activator of NF-κB ligand/osteoprotegerin (OPG) ratio and an increase in OPG mRNA expression. Additionally, the increased mRNA expression of the calcitonin receptor during P-restriction points to a higher number of osteoclasts. This study demonstrates an impairment of bone remodelling processes in young goats by N- or P-restriction. With P-restriction, bone mineralisation rate was potentially reduced and bone quality impaired, while with N-restriction, bone remodelling increased.

This study aimed to investigate the relationship between bone quality in terms of metabolism, homeostasis of elements, bone mineral density (BMD), and microstructure and keel-bone fractures in laying hens (Gallus gallus domesticus). One hundred and twenty 17 week old Lohmann White laying hens with normal keel bones were individually housed in furnished cages for 25 weeks. Birds were then euthanased and dissected to assess keel-bone status at 42 weeks. Serum and keel-bone samples from normal keel (NK) and fractured keel (FK) hens were collected to determine the previously mentioned bone quality parameters. The results showed FK hens to have higher levels of the components of osteocalcin, greater alkaline phosphatase activity in serum and keel bones, and greater tartrate-resistant acid phosphatase (TRAP) activity in keel bones, compared to NK hens. Additionally, FK hens also had higher concentrations of Li, B, K, Cu, As, Se, Sn, Hg, and Pb, but lower concentrations of Na, P, and Ca. Moreover, FK hens showed decreased bone microstructural parameters including bone volume/tissue volume, trabecular number, degree of anisotropy, connectivity density, and BMD, but increased trabecular separation. Meanwhile, no differences were detected in serum TRAP activity, trabecular thickness, bone surface, or bone surface/bone volume. Results showed laying hens with keel-bone fractures to have differences in bone metabolism, elements of home-ostasis, bone microstructure parameters, and BMD. These results suggest that keel-bone fractures may be associated with bone quality.

Recently it has been demonstrated that there are differences between sheep and goats in respect to adaptation to a calcium-restricted diet. It was the aim of the present study to evaluate whether species-specific peculiarities also occur when calcium homoeostasis is challenged by lactation. Therefore, we investigated the time courses of plasma parameters related to calcium homoeostasis (calcium, phosphate, calcitriol, the bone resorption marker CrossLaps® and the bone formation marker osteocalcin) during the transition period in multiparous animals of both species and compared the results to data from a former study carried out with dairy cows. As in cows, plasma calcium and the ratio of bone formation to bone resorption decreased at parturition in goats while plasma calcitriol increased. On day 10 post partum the bone parameters of goats reached prepartum values again, which was not the case in cows. Sheep were found to experience a challenge of calcium homoeostasis already 10 d before parturition, reflected by a very low ratio of bone formation to bone resorption, which was not accompanied by an increase in plasma calcitriol. Additionally, sheep and goats which had been in milk for 3 months were sampled, dried-off and sampled again 6 weeks later. In dried-off animals there were no detectable differences in parameters of bone metabolism. In conclusion we could show that the contribution of bone mobilisation to the compensation for the enhanced calcium demand due to lactation differs between the three ruminant species.

Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22–30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and bone metabolism were followed. Potassium citrate decreased the bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in bone formation marker (bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently.

Recent research has provided insights into dietary components that may optimise bone health and stimulate bone formation. Fruit and vegetable intake, as well as grains and other plant-derived food, have been linked to decreased risk of major chronic diseases including osteoporosis. This effect has been partially attributed to the polyphenols found in these foods. Thus, it has been suggested that these compounds may provide desirable bone health benefits through an action on bone cell metabolism. The present review will focus on how some polyphenols can modulate osteoblast function and reports which cellular signalling pathways are potentially implicated. However, to date, despite numerous investigations, few studies have provided clear evidence that phenolic compounds can act on osteoblasts. Polyphenols cited in the present review seem to be able to modulate the expression of transcription factors such as runt-related transcription factor-2 (Runx2) and Osterix, NF-κB and activator protein-1 (AP-1). It appears that polyphenols may act on cellular signalling such as mitogen-activated protein kinase (MAPK), bone morphogenetic protein (BMP), oestrogen receptor and osteoprotegerin/receptor activator of NF-κB ligand (OPG/RANKL) and thus may affect osteoblast functions. However, it is also important to take in account the possible interaction of these compounds on osteoclast metabolism to better understand the positive correlation reported between the consumption of fruit and vegetables and bone mass.

Osteoporosis is a major public health problem, and as life expectancy and the world's population continue to increase will become even more important. Thus, there is an urgent need to develop and implement nutritional approaches and policies for the prevention and treatment of osteoporosis. Patients with some chronic inflammatory diseases appear to be more likely to develop osteopenia, and in some cases earlier in life, which is of particular concern as the incidence of inflammatory diseases in the Western world is increasing. While the cause of bone loss in patients with inflammatory disease is multifactorial, nutrition may have a role. Many of these patients may have one or more nutritional deficiencies, which can lead to altered rates of bone metabolism. On the other hand, some nutritional factors may attenuate the inflammatory process itself, and thus may indirectly benefit bone metabolism and bone health in patients with inflammatory disease. The present review will consider these issues, particularly in the context of inflammatory bowel disease, coeliac diease and atherosclerosis.

Skeletal injuries in the equine athlete are a tremendous concern with both economic and animal welfare implications. As a result, much research has focused on improving bone quality through nutritional and exercise interventions. With the recent utilization of biochemical markers, changes in bone metabolism can be monitored. This study examined and compared the response of bone markers and estimates of bone mineral content, in studies with nutritional interventions, with those utilizing exercise interventions. The post hoc analyses suggest that nutritional interventions result in less change to bone markers and bone mineral content than exercise treatments. Of the bone markers examined, osteocalcin correlates most strongly to estimates of bone quality while keratin sulphate, an indicator of cartilage turnover, showed the least correlation. Comparing the results of this study with other published studies, similar findings were observed, suggesting that small alterations in exercise play a greater role in affecting measurable changes in bone metabolism and quality of the equine athlete than do small changes in nutrition.

A high dietary P intake is suggested to have negative effects on bone through increased parathyroid hormone secretion, as high serum parathyroid hormone (S-PTH) concentration increases bone resorption. In many countries the P intake is 2- to 3-fold above dietary guidelines, whereas Ca intake is too low. This combination may not be optimal for bone health. In a previous controlled study, we found that dietary P dose-dependently increased S-PTH and bone resorption and decreased bone formation. The aim of the present study was to investigate the dose–response effects of Ca intake on Ca and bone metabolism with a dietary P intake higher than recommended. Each of the twelve healthy female subjects aged 21–40 years attended three 24-h study sessions, which were randomized with regard to a Ca dose of 0 (control day), 600 or 1200 mg, and each subject served as her own control. The meals on each study day provided 1850 mg P and 480 mg Ca. S-PTH concentration decreased (P < 0·001) and serum ionized Ca concentration increased (P < 0·001) with increasing Ca doses. The bone formation marker, serum bone-specific alkaline phosphatase, did not differ significantly (P = 0·4). By contrast, the bone resorption marker, urinary N-terminal telopeptide of collagen type I, decreased significantly with both Ca doses (P = 0·008). When P intake was above current recommendations, increased Ca intake was beneficial for bone, as indicated by decreased S-PTH concentration and bone resorption. However, not even a high Ca intake could affect bone formation when P intake was excessive.

Ca and P are both essential nutrients for bone and are known to affect one of the most important regulators of bone metabolism, parathyroid hormone (PTH). Too ample a P intake, typical of Western diets, could be deleterious to bone through the increased PTH secretion. Few controlled dose–response studies are available on the effects of high P intake in man. We studied the short-term effects of four P doses on Ca and bone metabolism in fourteen healthy women, 20–28 years of age, who were randomized to four controlled study days; thus each study subject served as her own control. P supplement doses of 0 (placebo), 250, 750 or 1500mg were taken, divided into three doses during the study day. The meals served were exactly the same during each study day and provided 495mg P and 250mg Ca. The P doses affected the serum PTH (S-PTH) in a dose-dependent manner (P=0·0005). There was a decrease in serum ionized Ca concentration only in the highest P dose (P=0·004). The marker of bone formation, bone-specific alkaline phosphatase, decreased (P=0·05) and the bone resorption marker, N-terminal telopeptide of collagen type I, increased in response to the P doses (P=0·05). This controlled dose–response study showed that P has a dose-dependent effect on S-PTH and increases PTH secretion significantly when Ca intake is low. Acutely high P intake adversely affects bone metabolism by decreasing bone formation and increasing bone resorption, as indicated by the bone metabolism markers.

This study evaluated the effect of a fat blend containing long-chain (LC) n-3 PUFA on bone mineral density (BMD) and bone metabolism in gonad-intact middle-aged male rats (12 months old, n 28). Seven rats were killed on day 0 of dietary intervention to determine the baseline BMD. The remaining rats (seven per group) were fed a diet with one of the following dietary lipid treatments (g/kg diet): 167g safflower oil+33g menhaden oil (N6+N3 diet, control), 200g safflower oil (N6 diet, almost devoid of LC n-3 PUFA), or 190g menhaden oil+10g corn oil (N3 diet, rich in LC n-3 PUFA) for 20 weeks. After 20 weeks, all dietary treatment groups had a lower BMD compared with the baseline reference. However, rats fed the N3 diet had the highest bone mineral content and cortical+subcortical BMD compared with those fed the N6 and control N6+N3 diet. Compared with the control (N6+N3) group, rats fed the N3 diet had higher values for serum insulin-like growth factor-I, parathyroid hormone, 1, 25-(OH)2 vitamin D3 and bone-specific alkaline phosphatase activity, but lower bone NO production and urinary Ca, whereas rats fed the N6 diet had higher bone prostaglandin E2 production and serum pyridinoline. These findings indicate a protective action of LC n-3 PUFA on ageing-induced bone loss in gonad-intact middle-aged male rats through a modulation of local factors and systemic calcitrophic hormones.

The influence of a high-Na, high-protein (calciuric) diet on Ca and bone metabolism was investigated in postmenopausal women (aged 50–67 years) who were stratified by vitamin D receptor (VDR) genotype. In a crossover trial, twenty-four women were randomly assigned to a diet high in protein (90 g/d) and Na (180 mmol/d) or a diet adequate in protein (70 g/d) and low in Na (65 mmol/d) for 4 weeks, followed by crossover to the alternative dietary regimen for a further 4 weeks. Dietary Ca intake was maintained at usual intakes (about 20 mmol (800 mg)/d). Urinary Na, K, Ca, N and type I collagen cross-linked N-telopeptide (NTx; a marker of bone resorption), plasma parathyroid hormone (PTH), serum 25-hydroxycholecalciferol (25(OH)D3), 1,25-dihydroxycholecalciferol (1,25(OH)2D3), osteocalcin and bone-specific alkaline phosphatase (B-Alkphase) were measured in 24 h urine samples and fasting blood samples collected at the end of each dietary period. The calciuric diet significantly (P<0·05) increased mean urinary Na, N, K, Ca and NTx (by 19 %) compared with the basal diet, but had no effect on circulating 25(OH)D3, 1,25(OH)2D3, PTH, osteocalcin or B-Alkphase in the total group (n 24). There were no differences in serum markers or urinary minerals between the basal and calciuric diet in either VDR genotype groups. While the calciuric diet significantly increased urinary NTx (by 25·6 %, P<0·01) in the f+ VDR group (n 10; carrying one or more (f) Fok I alleles), it had no effect in the f− VDR group (n 14; not carrying any Fok I alleles). It is concluded that the Na- and protein-induced urinary Ca loss is compensated for by increased bone resorption and that this response may be influenced by VDR genotype.

The effect of polyunsaturated fatty acids (PUFA), in particular conjugated linoleic acid (CLA), on Ca and bone metabolism is unclear. In a 2 × 2 factorial design study, forty male 4-week-old rats were fed a control diet containing 70 g added fat (soyabean oil (SBO; n–6 PUFA-rich diet) or menhaden oil–safflower oil (MSO; n−3 PUFA-rich diet))/kg diet with 0 or 10 g CLA/kg for 8 weeks. Ex vivo prostaglandin E2biosynthesis by bone organ culture was significantly higher (P<0·001) in rats consuming SBO compared with MSO, irrespective of CLA. Addition of the CLA treatment to either diet further lowered (P<0·05) ex vivo prostaglandin E2 production. Neither PUFA type nor CLA altered circulating or femoral mRNA levels of osteocalcin (a marker of bone formation) or insulin-like growth factor-I (a mediator of bone metabolism). While urinary pyridinium crosslinks levels (markers of bone resorption) were unaffected by CLA irrespective of PUFA type, they were significantly higher (P<0·05) in rats consuming SBO compared with MSO irrespective of CLA. Net fractional (%) and absolute (mg) Ca absorption were significantly (P<0·01 and P<0·05 respectively) higher in CLA-supplemented than unsupplemented animals fed on the n−3 PUFA-rich diet, whereas CLA had no effect in animals fed the n–6 PUFA-rich diet. There was no effect of CLA supplementation on bone mineral mass. In conclusion, CLA supplementation over 8 weeks appeared to enhance Ca absorption in young growing rats fed an n−3 PUFA-rich diet, but had no measurable effect on bone metabolism or bone mass over this time frame.