“…The sites for nucleation and mineral deposition within the protein matrix of bone are geometric features intrinsic to the 640 A repeat crystal lattice of collagen (53). This "nucleation theory" is strengthened by the demlonstration that maturationl and increased cross-linking of newly synthesized collagen preceeds calcification (25,54). It is also supported by the observation that the altered maturational sequence of bone collagen attending experimental lathrytic states is characterized by an increase in the immature ACP mineral fraction.…”
A B S T R A C T The effect of chronic renal disease on bone matrix and mineral maturation was evaluated in rats with experimental renal insufficiency of 2-11 wk duration utilizing bromoform-toluene gradient fractionation of bone powder, pulse labeling experiments with "5Ca and proline-'H differential extraction, an(d X-ray diffraction techniques.Maturation defects in both collagen and minieral (45Ca) metabolism were documented as early as 2 wk after the induction of uremia, when total bone calcium, inorganic phosphate, and hydroxyproline content were unchanged.The maturational defect progressed with advancing uremia despite insignificant changes in plasma pH and calcium, and normal bone carbonate levels.Although circulating levels of 25-hydroxycholecalciferol were significantly lower than normal in the uremic animals, pretreatment with either this vitamin D metabolite or vitamin D3 itself failed to alter the observed changes in skeletal maturation.
INTRODUCTIONChronic renal failure is attended by a metabolic acidosis, intestinal malabsorption of amino acids (1) and minerals, alterations in vitamin D3 metabolism as well as increased circulating levels of parathyroid hormone, and uremic toxins such as indoles and guanidines. These biological derangements either singularly or in concert result in a form of osteopenia which because of its varied histological manifestation is termed "renal osteodys-
“…The sites for nucleation and mineral deposition within the protein matrix of bone are geometric features intrinsic to the 640 A repeat crystal lattice of collagen (53). This "nucleation theory" is strengthened by the demlonstration that maturationl and increased cross-linking of newly synthesized collagen preceeds calcification (25,54). It is also supported by the observation that the altered maturational sequence of bone collagen attending experimental lathrytic states is characterized by an increase in the immature ACP mineral fraction.…”
A B S T R A C T The effect of chronic renal disease on bone matrix and mineral maturation was evaluated in rats with experimental renal insufficiency of 2-11 wk duration utilizing bromoform-toluene gradient fractionation of bone powder, pulse labeling experiments with "5Ca and proline-'H differential extraction, an(d X-ray diffraction techniques.Maturation defects in both collagen and minieral (45Ca) metabolism were documented as early as 2 wk after the induction of uremia, when total bone calcium, inorganic phosphate, and hydroxyproline content were unchanged.The maturational defect progressed with advancing uremia despite insignificant changes in plasma pH and calcium, and normal bone carbonate levels.Although circulating levels of 25-hydroxycholecalciferol were significantly lower than normal in the uremic animals, pretreatment with either this vitamin D metabolite or vitamin D3 itself failed to alter the observed changes in skeletal maturation.
INTRODUCTIONChronic renal failure is attended by a metabolic acidosis, intestinal malabsorption of amino acids (1) and minerals, alterations in vitamin D3 metabolism as well as increased circulating levels of parathyroid hormone, and uremic toxins such as indoles and guanidines. These biological derangements either singularly or in concert result in a form of osteopenia which because of its varied histological manifestation is termed "renal osteodys-
“…For the determination of"H-radioactivity, 0.5 ml of the solution was diluted with 1.5 ml of distilled water, and calcium was precipitated with 0.5 ml of saturated ammonium oxalate at pH 5 (cf. Uitto & Laitinen 1968). An aliquot of the supernatant was used for the counting of total '<H-radioactivity (Prockop & Ebert 1963).…”
Section: Animals and Exprrimenrcil Conditionsmentioning
The effects of physical training on the metabolism of collagen, calcium and glycosaminoglycans in various connective tissues were studied in male NMRI mice. The mice to be trained and their controls were about 3 weeks old (expt. I) and 8 weeks old (expt. II) at the commencement of training. The training was performed on a 5 degree inclined treadmill 5 days a week for 4 weeks in expt. I and for 3 weeks in expt. II. The daily exercise time was progressively increased from 20 min in the first week up to 80 min in the third week. The incorporation of 3H-proline to collagen hydroxyproline was increased by training in long bones, skeletal muscle and Achilles tendon, whereas the incorporation of 35S-sulphate into glycosaminoglycans of bones was lower for the trained compared to the control mice. The differences between the two groups in the incorporation of 45calcium were negligible. The results indicate that the metabolism of collagen is accelerated by physical training in several connective tissues in young rapidly growing mice, whereas the metabolism of glycosaminoglycans remains uneffected or is even retarded.
“…These changes occurred well in advance of the inorganic structural alterations described in the present study. Since it is thought that maturation and increased cross-linking of newly synthesized collagen precedes calcification in hard tissues (15,16), the altered maturational sequence attending experimental chronic uremia suggests that normal cell processes are, at the very least, sequentially perturbed at the bone level. The relationship of these data to reports of altered vitamin D metabolism in uremia (17) and to others citing defective collagen cross-linking in the vitamin D-deficient state (18) are vet to be defined.…”
A B S T R A C T X-ray diffraction analysis of bone from chronically uremic but nonacidotic rats with normocalcemia and hyperphosphatemia revealed smaller apatite crystals and an increase in the X-ray amorphous mineral fraction when compared to age-matched, pair-fed control animals, indicating less advanced mineral maturation in the uremic animals. Studies in animals with varied degrees of chronic renal insufficiency revealed a progression of the bone crystal maturational defect with advancing uremia.
INTRODUCTIONAlthough a causal relationship between chronic renal failure and progressive osteopenia has been well documented by radiographic and histochemical analyses (1, 2), the sequence of physiology and biochemical events that initiate and perpetuate the derangements in skeletal metabolism are still poorly defined. Previous investigations have been concerned primarily with rates of bone mineral (apatite) and matrix (collagen) turnover, under the assumption that the intricate processes of crystal growth and collagen maturation were proceeding in normal fashion. In an earlier study, we demonstrated maturational alterations in bone collagen and mineral metabolism in the experimental uremic state that progressed with advancing uremia, although insignificant alterations in plasma pH, calcium, and bone carbonate content obtained (3). The present study was undertaken to determine whether the apparent collagen maturational defect in the advancing uremic state is associated with compositional and structural alterations of the mineral
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