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  • 1
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    Vitamin D deficiency and reproduction in rats (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-04-06
    Description: Female weanling rats from a colony maintained on a diet low in vitamin D were raised on a diet that was deficient in vitamin D but was otherwise adequate. Vitamin D deficiency was confirmed in the rats by hypocalcemia and the absence of vitamin D metabolites in blood. These females gave birth to litters that were slightly smaller than control litters from females maintained on a vitamin D-containing diet. The pups from the vitamin D-deficient mothers appeared normal throughout lactation, and at weaning had normal concentrations of calcium and phosphate in the plasma. These results indicate that vitamin D and its metabolites are not necessary for reproduction and fetal development in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halloran, B P -- DeLuca, H F -- New York, N.Y. -- Science. 1979 Apr 6;204(4388):73-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/432628" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Suckling/blood ; Body Weight ; Bone Development ; Calcium/blood ; Female ; Hydroxycholecalciferols/blood ; Phosphates/blood ; Rats ; *Reproduction ; Vitamin D Deficiency/blood/*physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
    Electronic Resource
    Electronic Resource
    Studies on the role of 24-hydroxylation of vitamin D in the mineralization of cartilage and bone of vitamin D-deficient rats (1981)
    Springer
    Calcified tissue international 33 (1981), S. 489-497 
    Details
    ISSN: 1432-0827
    Keywords: Vitamin D ; Vitamin D deficiency ; Cartilage ; Bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To test the importance of 24-hydroxylation of vitamin D3 on bone mineralization, rat pups born to vitamin D-deficient females were given either 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3 for 16 days beginning at the time of weaning. Following such treatment analysis of blood samples revealed no detectable 24R,25-(OH)2D3 and 1,25-(OH)2D3 in the rats given the difluoro compound while revealing the expected 24,24-difluoro-25-hydroxyvitamin D3 and 24,24-difluoro-1,25-dihydroxyvitamin D3. The rats given 25-hydroxyvitamin D3 had the expected levels of 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D3, and 1,25-dihydroxyvitamin D3. Following sacrifice at day 17, postweaning bone mineralization and modeling were studied in long bones using histological methods. Bones taken from vitamin D-deficient rats at the beginning and end of the experimental period had lesions typical of rickets. These included wide growth plates, excessive amounts of osteoid, and metaphyseal fibrosis. Following treatment with either 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3, bone mineralization returned to normal. Growth plate widths and the amount of osteoid on bone surfaces were both substantially reduced and to a similar degree in both treatment groups. Normal cartilage core formation and trabecularization of the metaphyseal primary spongiosa were also restored to a similar degree in both groups. In effect, no difference was observed in any bone parameter studied between the 25-hydroxyvitamin D3- and the 24,24-difluoro-25-hydroxyvitamin D3-treated animals. These results provide strong evidence that 24-hydroxylation of the vitamin D molecule plays little or no role in the modeling and mineralization of bone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02409479
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  • 3
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    Vitamin D metabolism during pregnancy and lactation in the rat. (1979)
    National Academy of Sciences
    Details
    Publication Date: 1979-11-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Osteoblast expression of an engineered Gs-coupled receptor dramatically increases bone mass (2008)
    National Academy of Sciences
    Details
    Publication Date: 2008-01-22
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    High levels of a parathyroid hormone-like protein in milk. (1989)
    National Academy of Sciences
    Details
    Publication Date: 1989-09-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Skeletal unloading decreases production of 1,25-dihydroxyvitamin D (1993)
    In:  Other Sources
    Details
    Publication Date: 2011-08-24
    Description: The plasma concentration of 1,25-dihydroxyvitamin D [1,25(OH)2D] decreases during skeletal unloading and increases when normal weight bearing is restored. To determine whether these changes in plasma 1,25(OH)2D reflect changes in production, metabolic clearance, or both we measured the kinetics of 1,25(OH)2D metabolism in rats whose skeletons were normally loaded, unloaded, or reloaded after a period of nonweight bearing. Skeletal unloading produced a transient but striking fall in the production (-73%) and plasma concentration (-72%) of 1,25(OH)2D without having a significant effect (〈 20%) on metabolic clearance. Skeletal reloading returned production to normal. Bone formation predictably decreased during unloading and returned to normal after return to weight bearing. No consistent changes in blood ionized calcium, plasma immunoreactive parathyroid hormone (irPTH), or plasma phosphorus occurred. These data suggest that the changes in plasma 1,25-(OH)2D associated with changes in skeletal weight bearing primarily reflect changes in 1,25(OH)2D production. The data provide no evidence that the changes in 1,25(OH)2D production are a consequence of changes in blood ionized calcium, plasma irPTH, or phosphorus.
    Keywords: Life Sciences (General)
    Type: The American journal of physiology (ISSN 0002-9513); Volume 264; 5 Pt 1; E712-6
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  • 7
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    Altered skeletal pattern of gene expression in response to spaceflight and hindlimb elevation (1994)
    In:  Other Sources
    Details
    Publication Date: 2011-08-24
    Description: Spaceflight leads to osteopenia, in part by inhibiting bone formation. Using an animal model (hindlimb elevation) that simulates the weightlessness of spaceflight, we and others showed a reversible inhibition of bone formation and bone mineralization. In this study, we have measured the mRNA levels of insulin-like growth factor I (IGF-I), IGF-I receptor (IGF-IR), alkaline phosphatase, and osteocalcin in the tibiae of rats flown aboard National Aeronautics and Space Administration Shuttle Flight STS-54 and compared the results with those obtained from their ground-based controls and from the bones of hindlimb-elevated animals. Spaceflight and hindlimb elevation transiently increase the mRNA levels for IGF-I, IGF-IR, and alkaline phosphatase but decrease the mRNA levels for osteocalcin. The changes in osteocalcin and alkaline phosphatase mRNA levels are consistent with a shift toward decreased maturation, whereas the rise in IGF-I and IGF-IR mRNA levels may indicate a compensatory response to the fall in bone formation. We conclude that skeletal unloading during spaceflight or hindlimb elevation resets the pattern of gene expression in the osteoblast, giving it a less mature profile.
    Keywords: Aerospace Medicine
    Type: The American journal of physiology (ISSN 0002-9513); Volume 267; 6 Pt 1; E822-7
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  • 8
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    The molecular response of bone to growth hormone during skeletal unloading: regional differences (1995)
    In:  Other Sources
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    Publication Date: 2011-08-24
    Description: Hind limb elevation of the growing rat provides a good model for the skeletal changes that occur during space flight. In this model the bones of the forelimbs (normally loaded) are used as an internal control for the changes that occur in the unloaded bones of the hind limbs. Previous studies have shown that skeletal unloading of the hind limbs results in a transient reduction of bone formation in the tibia and femur, with no change in the humerus. This fall in bone formation is accompanied by a fall in serum osteocalcin (bone Gla protein, BGP) and bone BGP messenger RNA (mRNA) levels, but a rise in bone insulin-like growth factor-I (IGF-I) protein and mRNA levels and resistance to the skeletal growth-promoting actions of IGF-I. To determine whether skeletal unloading also induced resistance to GH, we evaluated the response of the femur and humerus of sham and hypophysectomized rats, control and hind limb elevated, to GH (two doses), measuring mRNA levels of IGF-I, BGP, rat bone alkaline phosphatase (RAP), and alpha 1(1)-procollagen (coll). Hypophysectomy (HPX) decreased the mRNA levels of IGF-I, BGP, and coll in the femur, but was either less effective or had the opposite effect in the humerus. GH at the higher dose (500 micrograms/day) restored these mRNA levels to or above the sham control values in the femur, but generally had little or no effect on the humerus. RAP mRNA levels were increased by HPX, especially in the femur. The lower dose of GH (50 micrograms/day) inhibited this rise in RAP, whereas the higher dose raised the mRNA levels and resulted in the appearance of additional transcripts not seen in controls. As for the other mRNAs, RAP mRNA in the humerus was less affected by HPX or GH than that in the femur. Hind limb elevation led to an increase in IGF-I, coll, and RAP mRNAs and a reduction in BGP mRNA in the femur and either had no effect or potentiated the response of these mRNAs to GH. We conclude that GH stimulates a number of markers of bone formation by raising their mRNA levels, and that skeletal unloading does not block this response, but the response varies substantially from bone to bone.
    Keywords: Aerospace Medicine
    Type: Endocrinology (ISSN 0013-7227); Volume 136; 5; 2099-109
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  • 9
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    Bone and hormonal changes induced by skeletal unloading in the mature male rat (1999)
    In:  Other Sources
    Details
    Publication Date: 2011-08-24
    Description: To determine whether the rat hindlimb elevation model can be used to study the effects of spaceflight and loss of gravitational loading on bone in the adult animal, and to examine the effects of age on bone responsiveness to mechanical loading, we studied 6-mo-old rats subjected to hindlimb elevation for up to 5 wk. Loss of weight bearing in the adult induced a mild hypercalcemia, diminished serum 1,25-dihydroxyvitamin D, decreased vertebral bone mass, and blunted the otherwise normal increase in femoral mass associated with bone maturation. Unloading decreased osteoblast numbers and reduced periosteal and cancellous bone formation but had no effect on bone resorption. Mineralizing surface, mineral apposition rate, and bone formation rate decreased during unloading. Our results demonstrate the utility of the adult rat hindlimb elevation model as a means of simulating the loss of gravitational loading on the skeleton, and they show that the effects of nonweight bearing are prolonged and have a greater relative effect on bone formation in the adult than in the young growing animal.
    Keywords: Aerospace Medicine
    Type: The American journal of physiology (ISSN 0002-9513); Volume 276; 1 Pt 1; E62-9
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  • 10
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    Space flight and the skeleton: lessons for the earthbound (1997)
    In:  Other Sources
    Details
    Publication Date: 2011-08-24
    Description: Loss of bone during extended space flight has long been a concern that could limit the ability of humans to explore the universe. Surprisingly, the available data do not support the concept that weightlessness leads inexorably to a depleted skeleton unable to withstand the stress of a return to a 1-g environment. Nevertheless, some bone loss does occur, especially in those bones most stressed by gravity prior to flight, which provides confirmation of the proposal formulated over a century ago by Julius Wolff that mechanical stress determines the form and function of bone. Although the phenomenon of bone loss with skeletal unloading, whether by space flight or immobilization or just taking a load off your feet (literally) is well established, the mechanisms by which bone senses load and adjusts to it are not so clear. What actually is the stimulus, and what are the sensors? What are the target cells? How do the sensors communicate the message into the cells, and by what pathways do the cells respond? What is the role of endocrine, factors vs. paracrine or autocrine factors in mediating or modulating the response? None of these questions has been answered with certainty, but, as will become apparent in this review, we have some clues directing us to the answers. Although the focus of this review concerns space flight, it seems highly likely that the mechanisms mediating the transmission of mechanical load to changes in bone formation and resorption apply equally well to all forms of disuse osteoporosis and are likely to be the same mechanisms affected by other etiologies of osteoporosis.
    Keywords: Aerospace Medicine
    Type: The Endocrinologist (ISSN 1051-2144); Volume 7; 1; 10-22
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