acid-phosphatase and Malnutrition

The role of iron (Fe) in bone formation and disease have not received much attention, a fact that is interesting given the known biochemical role that this mineral has upon collagen maturation together with the high prevalence of Fe-deficiency anaemia worldwide.. To investigate the changes in bone formation, resorption and mineral content in developing rats with induced nutritional Fe-deficiency anaemia.. Thirty male Wistar rats were divided into two groups, a control group receiving AIN-93G diet with normal-Fe content and an anaemic group receiving AIN-93G diet with low-Fe content for 40 days. Both diets were prepared with an adequate calcium (Ca) and phosphorus (P) content. The most representative serum bone turnover biomarkers and femur and sternum calcium and phosphorus content, together with sternum Fe content were determined in both experimental groups.. In anaemic rats, bone matrix formation diminished as revealed by the lower amount of procollagen type I N-terminal propeptide. Bone resorption process increased in Fe deficiency as shown by the increase of serum parathyroid hormone, tartrate-resistant acid phosphatase and levels of degradation products from C-terminal telopeptides of type I collagen released to the serum. In addition, mineralization process was affected by Fe deficiency, because Ca and P content in femur decreased markedly.. Fe-deficiency anaemia had a significant impact upon bone, affecting bone mineralization, decreasing the matrix formation and increasing bone resorption, therefore it is of great interest to assess bone status in situation of Fe-deficiency anaemia.

Topics: Acid Phosphatase; Anemia, Iron-Deficiency; Animals; Biomarkers; Bone and Bones; Calcification, Physiologic; Calcium, Dietary; Diet; Femur; Ferritins; Iron, Dietary; Isoenzymes; Male; Malnutrition; Parathyroid Hormone; Phosphorus; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Vitamin D

The phosphate signal transduction (PHO) pathway, which regulates genes in response to phosphate starvation, is well defined in Saccharomyces cerevisiae. We asked whether the PHO pathway was the same in the distantly related fission yeast Schizosaccharomyces pombe. We screened a deletion collection for mutants aberrant in phosphatase activity, which is primarily a consequence of pho1(+) transcription. We identified a novel zinc finger-containing protein (encoded by spbc27b12.11c(+)), which we have named pho7(+), that is essential for pho1(+) transcriptional induction during phosphate starvation. Few of the S. cerevisiae genes involved in the PHO pathway appear to be involved in the regulation of the phosphate starvation response in S. pombe. Only the most upstream genes in the PHO pathway in S. cerevisiae (ADO1, DDP1, and PPN1) share a similar role in both yeasts. Because ADO1 and DDP1 regulate ATP and IP(7) levels, we hypothesize that the ancestor of these yeasts must have sensed similar metabolites in response to phosphate starvation but have evolved distinct mechanisms in parallel to sense these metabolites and induce phosphate starvation genes.

Topics: Acid Phosphatase; Carbon; Epistasis, Genetic; Evolution, Molecular; Fungal Proteins; Gene Deletion; Gene Expression Profiling; Gene Expression Regulation, Fungal; Intracellular Signaling Peptides and Proteins; Malnutrition; Nitrogen; Phenotype; Phosphates; Phosphoric Monoester Hydrolases; Schizosaccharomyces; Transcription Factors