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  • American Physiological Society  (6)
  • 1
    Online Resource
    Online Resource
    Increased clearance of 1,25(OH)2D3 and tissue-specific responsiveness to 1,25(OH)2D3 in diabetic rats
    American Physiological Society ; 1993
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 265, No. 2 ( 1993-08-01), p. E215-E223
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 265, No. 2 ( 1993-08-01), p. E215-E223
    Abstract: The kinetics of 1,25-dihydroxyvitamin D3 [1,25(OH)2-D3] and the in vivo response to 1,25(OH)2D3 (7.5, 15, and 30 ng/100 g body wt), infused or injected subcutaneously for 12-14 days, were studied in male spontaneously diabetic and control BB rats. In control rats, increasing doses of 1,25(OH)2D3 produced parallel increases in plasma 1,25(OH)2D3 and calcium, urinary calcium, duodenal CaBP9K, and renal CaBP28K. 1,25-(OH)2D3 at 30 ng/100 g markedly raised plasma osteocalcin and osteoblast/osteoid surfaces in the tibial metaphysis, but inhibited bone mineralization rate. In diabetic rats, plasma 1,25-(OH)2D3 concentrations were decreased, and the rise of plasma 1,25(OH)2D3 during 1,25(OH)2D3 infusion was blunted, but the free 1,25(OH)2D3 index remained normal or above normal. Diabetic rats had an increased metabolic clearance rate of 1,25-(OH)2D3 (0.38 +/- 0.015 vs. 0.24 +/- 0.007 ml.min-1.kg-1), with no further increase in 1,25(OH)2D3-infused diabetic rats; their relative production rate of 1,25(OH)2D3 was unchanged. The responses of plasma and urinary calcium, duodenal CaBP9K, and renal CaBP28K to infused 1,25(OH)2D3 were normal, as was duodenal calcium absorption in 1,25(OH)2D3-injected diabetic rats. However, the virtual absence of osteoblasts/osteoid in trabecular bone was unaltered in diabetic rats infused with 30 ng/100 g 1,25(OH)2D3, with only minimal increase of their low plasma osteocalcin levels. 1,25(OH)2D3 treatment therefore cannot be expected to reverse diabetic osteopenia.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1993.265.2.E215
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1477331-4
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  • 2
    Online Resource
    Online Resource
    Binding protein for vitamin D and its metabolites in rat mesenteric lymph
    American Physiological Society ; 1985
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 249, No. 1 ( 1985-07-01), p. E1-E5
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 249, No. 1 ( 1985-07-01), p. E1-E5
    Abstract: A protein with high affinity for vitamin D3 and 25-hydroxyvitamin D3 in rat mesenteric lymph has been studied. Mesenteric lymph was collected after duodenal instillation of radiolabeled vitamin D3 and 25-hydroxyvitamin D3. As previously described, approximately 10% of vitamin D3 (S. Dueland, J.I. Pedersen, P. Helgerud, and C.A. Drevon, J. Biol. Chem. 257: 146-150, 1982) and 95% of 25-hydroxyvitamin D3 (S. Dueland, J.I. Pedersen, P. Helgerud, and C.A. Drevon, Am. J. Physiol. 245 (Endocrinol. Metab. 8): E463-E467, 1983) recovered in mesenteric lymph were associated with the alpha-globulin fractions. The radioactive vitamin D3 recovered in the lymph fraction with d greater than 1.006 (free of chylomicrons) coeluted with purified rat serum binding protein for vitamin D and its metabolites (DBP) from an antirat DBP column. The results obtained by immunoblotting after sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that this protein in mesenteric lymph had molecular weight and immunological properties identical with purified serum DBP. Purified serum DBP labeled with 125I was injected intravenously and mesenteric lymph was collected. in lymph, suggesting that DBP may be transferred from blood to mesenteric lymph and that plasma and lymph DBP may have a similar origin.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1985.249.1.E1
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1985
    detail.hit.zdb_id: 1477331-4
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  • 3
    Online Resource
    Online Resource
    Estrogens and Androgens in Skeletal Physiology and Pathophysiology
    American Physiological Society ; 2017
    In:  Physiological Reviews Vol. 97, No. 1 ( 2017-01), p. 135-187
    Details
    In: Physiological Reviews, American Physiological Society, Vol. 97, No. 1 ( 2017-01), p. 135-187
    Abstract: Estrogens and androgens influence the growth and maintenance of the mammalian skeleton and are responsible for its sexual dimorphism. Estrogen deficiency at menopause or loss of both estrogens and androgens in elderly men contribute to the development of osteoporosis, one of the most common and impactful metabolic diseases of old age. In the last 20 years, basic and clinical research advances, genetic insights from humans and rodents, and newer imaging technologies have changed considerably the landscape of our understanding of bone biology as well as the relationship between sex steroids and the physiology and pathophysiology of bone metabolism. Together with the appreciation of the side effects of estrogen-related therapies on breast cancer and cardiovascular diseases, these advances have also drastically altered the treatment of osteoporosis. In this article, we provide a comprehensive review of the molecular and cellular mechanisms of action of estrogens and androgens on bone, their influences on skeletal homeostasis during growth and adulthood, the pathogenetic mechanisms of the adverse effects of their deficiency on the female and male skeleton, as well as the role of natural and synthetic estrogenic or androgenic compounds in the pharmacotherapy of osteoporosis. We highlight latest advances on the crosstalk between hormonal and mechanical signals, the relevance of the antioxidant properties of estrogens and androgens, the difference of their cellular targets in different bone envelopes, the role of estrogen deficiency in male osteoporosis, and the contribution of estrogen or androgen deficiency to the monomorphic effects of aging on skeletal involution.
    Type of Medium: Online Resource
    ISSN: 0031-9333 , 1522-1210
    URL: Article
    DOI: 10.1152/physrev.00033.2015
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1471693-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    1,25(OH)2D3 and Ca-binding protein in fetal rats: relationship to the maternal vitamin D status
    American Physiological Society ; 1988
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 254, No. 4 ( 1988-04-01), p. E505-E512
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 254, No. 4 ( 1988-04-01), p. E505-E512
    Abstract: The autonomy and functional role of fetal 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] were investigated in nondiabetic and diabetic BB rats fed diets containing 0.85% calcium-0.7% phosphorus or 0.2% calcium and phosphorus and in semistarved rats on the low calcium-phosphorus diet. The changes in maternal and fetal plasma 1,25(OH)2D3 were similar: the levels were increased by calcium-phosphorus restriction and decreased by diabetes and semistarvation. Maternal and fetal 1,25(OH)2D3 levels were correlated (r = 0.80; P less than 0.001). The vitamin D-dependent calcium-binding proteins (CaBP9K and CaBP28K) were measured in multiple maternal and fetal tissues and in the placenta of nondiabetic, diabetic, and calcium-phosphorus-restricted rats. The distributions of CaBP9K and CaBP28K in the pregnant rat were similar to that of the growing rat. The increased maternal plasma 1,25(OH)2D3 levels in calcium-phosphorus-restricted rats were associated with higher duodenal CaBP9K and renal CaBPs, but placental CaBP9K was not different. In diabetic pregnant rats, duodenal CaBP9K tended to be lower, while renal CaBPs were normal; placental CaBP9K was decreased. No significant changes in CaBP levels were observed in fetuses of low calcium-phosphorus diet rats or fetuses of diabetic rats. The results indicate that in the rat fetal 1,25(OH)2D3 depends on maternal 1,25(OH)2D3 or on factors regulating maternal 1,25(OH)2D3. The lack of changes in fetal CaBP in the presence of altered fetal plasma 1,25(OH)2D3 levels confirms earlier data showing that 1,25(OH)2D3 has a limited hormonal function during perinatal development in the rat.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1988.254.4.E505
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Actions of Insulin and the IGFs on Bone
    American Physiological Society ; 1994
    In:  Physiology Vol. 9, No. 1 ( 1994-02-01), p. 20-22
    Details
    In: Physiology, American Physiological Society, Vol. 9, No. 1 ( 1994-02-01), p. 20-22
    Abstract: Insulin and insulin-like growth factors (IGF) I and II have receptors in osteoblastic cells and stimulate both their proliferation and activity in vitro. Insulin probably has no effect on osteoblast precursors. Osteoclast formation is induced by IGF-I in vitro, and IGF-I may affect bone (re)modeling in vivo.
    Type of Medium: Online Resource
    ISSN: 1548-9213 , 1548-9221
    URL: Article
    DOI: 10.1152/physiologyonline.1994.9.1.20
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 3115360-4
    detail.hit.zdb_id: 2005759-3
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  • 6
    Online Resource
    Online Resource
    Diabetes and low Ca-P diet have opposite effects on adult and fetal bone mineral metabolism
    American Physiological Society ; 1988
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 254, No. 4 ( 1988-04-01), p. E496-E504
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 254, No. 4 ( 1988-04-01), p. E496-E504
    Abstract: The effect of diabetes on maternal bone mineral metabolism and fetal mineralization was studied in nonpregnant and pregnant BB rats fed two diets (0.85% calcium-0.7% phosphorus and 0.2% calcium-phosphorus). Non-pregnant female diabetic rats had normal total bone mineral content (BMC), despite decreased trabecular bone volume density (TBVD). Nondiabetic rats on the low calcium-phosphorus diet showed decreased TBVD, signs of increased bone turnover, and decreased BMC; plasma 1,25-dihydroxyvitamin D3 [1,25 (OH)2D3] was increased and urinary calcium excretion was decreased. A similar response was observed in diabetic rats with a further decrease in TBVD. Nondiabetic 21-day pregnant rats on high and low calcium-phosphorus diets had higher 1,25(OH)2D3 than nonpregnant rats (98 vs. 58 and 328 vs. 147 pg/ml, respectively). Maternal BMC did not change during pregnancy but was decreased by the low calcium-phosphorus diet; fetal mineral content was not influenced by the low calcium-phosphorus regime. No increase in 1,25(OH)2D3 was observed in pregnant diabetic rats (57 vs. 52 and 112 vs. 128 pg/ml in high and low calcium-phosphorus diet groups). Fetal mineralization was severely impaired in diabetes but was not further decreased by the low calcium-phosphorus diet. Thus nonpregnant diabetic rats respond normally to a low calcium-phosphorus diet, but pregnant diabetic rats do not show increased 1,25(OH)2D3 levels due to impairment of fetal mineralization.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1988.254.4.E496
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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