Prenatal influences on bone health in children.

INTRODUCTION: Optimising bone health might reduce the burden of both fractures in childhood and fragility fractures in later life. A number of maternal dietary and non-dietary factors have been identified that might influence offspring bone health and represent targets for intervention. AREAS COVERED: This article will outline the accrual of bone mineral throughout the life course and how observational and intervention studies have shown that maternal diet, in particular maternal calcium and 25-hydroxyvitamin D [25(OH)D] status, and lifestyle are associated with offspring bone mineralization. Studies examining the effects of maternal micronutrient supplementation on offspring bone mineral density (BMD) will also be discussed. EXPERT COMMENTARY: There is a wealth of observational evidence relating maternal diet to offspring BMD. However, high quality randomized controlled trials, such as the ongoing MAVIDOS study, are needed before these findings can be definitively translated into public health advice.

XX Congreso SEIOMM: Bilbao 21-23 de Octubre 2015 / No disponible

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Protein nutrition as therapy for a genetic disorder of bone?

Bone formation is controlled by a network of transcription factors and signaling molecules. In this issue, , studying the role of the transcription factor ATF4 in a new mouse model of neurofibromatosis type I skeletal defects, demonstrate striking effects of changing dietary protein on bone formation abnormalities.

ATF4 mediation of NF1 functions in osteoblast reveals a nutritional basis for congenital skeletal dysplasiae.

The transcription factor ATF4 enhances bone formation by favoring amino acid import and collagen synthesis in osteoblasts, a function requiring its phosphorylation by RSK2, the kinase inactivated in Coffin-Lowry Syndrome. Here, we show that in contrast, RSK2 activity, ATF4-dependent collagen synthesis, and bone formation are increased in mice lacking neurofibromin in osteoblasts (Nf1(ob)(-/-) mice). Independently of RSK2, ATF4 phosphorylation by PKA is enhanced in Nf1(ob)(-/-) mice, thereby increasing Rankl expression, osteoclast differentiation, and bone resorption. In agreement with ATF4 function in amino acid transport, a low-protein diet decreased bone protein synthesis and normalized bone formation and bone mass in Nf1(ob)(-/-) mice without affecting other organ weight, while a high-protein diet overcame Atf4(-/-) and Rsk2(-/-) mice developmental defects, perinatal lethality, and low bone mass. By showing that ATF4-dependent skeletal dysplasiae are treatable by dietary manipulations, this study reveals a molecular connection between nutrition and skeletal development.

[Value of a phosphorus supplemented formula for premature infants]. / Intérêt d'une augmentation de l'apport phosphoré dans un lait pour le prématuré.

The fortuitous discovery of bone mineralization abnormalities in premature babies fed a medium chain triglyceride supplemented formula and exhibiting satisfactory weight gains prompted us to perform calcium and phosphorus balance studies. The infants studied had no major neonatal disorders and were not vitamin D-deficient. Urine assays detected no phosphorus and demonstrated an increase in calcium excretion, suggesting an inadequate phosphorus intake. This hypothesis was confirmed by the appearance of urinary phosphates with a decrease in calcium losses following supplementation of the formula with phosphorus.

The effects of manganese, biotin, and choline on hexosamine and hydroxyproline content as related to leg weakness.

Three experiments were conducted with day-old broiler chicks to determine the effects of dietary choline, biotin, and manganese on cartilage hexosamine and hydroxyproline content. The incidence of leg weakness was 75% or higher on all basal diets. The levels of supplementation found to minimize leg weakness were 1540 mg choline chloride/kg diet, .2 mg biotin/kg diet, and 100 mg manganese/kg diet. The levels required to maintain normal epiphyseal cartilage hexosamine content were 385 mg of choline chloride, .05 mg of biotin, and 25 mg of manganese/kg of diet. Substantially higher levels of nutrients were needed to reduce the incidence of leg weakness. Only with manganese supplementation was the incidence of leg weakness significantly reduced at the level of supplementation required for normal hexosamine content. Hydroxyproline content was not affected by varying the levels of supplemental choline, biotin, or manganese.

Influence of high levels of pyridoxine on twisted legs in broilers.

Three experiments were conducted using commercially available broiler chicks to study the influence of high levels of pyridoxine on incidence of twisted legs. Chicks were grown in wire floored battery brooders to two weeks of age when they were weighed and visually scored for twisted legs. Supplementation of a diet containing 2.2 mg synthetic vitamin B6/kg with 10 and 20 mg/kg pyridoxine resulted in a significant decrease (P less than or equal to .05) in incidence of twisted legs in Experiment 1. In Experiment 2, supplementation with 30, 60, or 100 mg/kg numerically reduced incidence, but the differences were not statistically significant. Incidence of twisted legs was significantly increased by injecting chicks with .5 ml physiological saline at 1 and 7 days of age in comparison to noninjected controls. Including 10 mg pyridoxine HCl in the saline reduced the incidence but it was still numerically higher than the noninjected controls. Factors other than vitamin B6 nutrition appear to play a more important role in the etiology of twisted legs in broiler chicks.

Foreleg lameness in rapidly growing dogs.

Foreleg lameness caused by the interaction of diet and rapid growth rate is all too frequently encountered in the large and giant breeds of dogs. In this paper, the influence of rapid growth rate and growth hormone on bone formation is briefly considered. The importance causes of this problem are discussed. These are hypertrophic osteodystrophy, osteodystrophy II, retained enchondral cartilage cores, panosteitis an nutritional secondary hyperparathyroidism. Rickets and hypertrophic pulmonary osteoarthropathy are also considered. Emphasis is placed on the aetiology, radiographic diagnosis and rational treatment. A case report of a 6-month-old Great Dane with osteodystrophy II and retained enchondral cartilage cores in the ulnar metaphyses is presented as an example of such a problem.

Bent-limb syndrome in lambs raised in total confinement.

A bent-limb syndrome in lambs raised in total confinement was characterized by curvature of the forelimbs. Radiographic findings included flaring of the affected long bone and thinning of the growth plate. The main histologic change was endochondral dysplasia of the long bone. In feed samples, all trace minerals analyzed were within recommended concentrations except iron, which was much higher (400 ppm dry matter) than the normal requirement of lambs (70 ppm). All mineral concentrations in serum were normal except those of inorganic phosphorus and iron, which were higher. Results of soft tissue and bone mineral analyses were normal. Altering the ratio of calcium and phosphorus did not affect the incidence of disease, but intramuscular administration of massive doses of vitamin D3 and reducing the amount of dietary iron had a prophylactic effect. The increase in serum phosphorus was probably related to the dietary excess of iron, which probably decreased vitamin D metabolite formation in the kidney, which in turn could be prevented by massive doses of vitamin D3.