Effect of Age on Calcium Absorption

Bullamore, J.R.; Wilkinson, Robert H.; Gallagher, J. Christopher; Nordin, B. E. C.; Marshall, D. H.

doi:10.1016/s0140-6736(70)91344-9

Cited by 410 publications

(132 citation statements)

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“…Thus, in healthy Caucasian men, the falls in calcium absorption efficiency and 24-h urinary calcium with age do not appear to be related to a fall in serum calcitriol. The demonstrated fall in intestinal calcium absorption with age is consistent with previous reports in normal men in which calcium absorption was measured using either single (Bullamore et al, 1970;Francis et al, 1989;Agnusdei et al, 1998), dual (Gallagher et al, 1979) isotope or strontium (Fatayerji et al, 2000) techniques. Our method uses a single isotope and a blood sample taken 1 h after the calcium dose, and, at this dose, measures active calcium transport.…”

Section: Discussionsupporting

confidence: 90%

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Relation between calcium absorption and serum calcitriol in normal men: evidence for age-related intestinal resistance to calcitriol

et al. 2004

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Objective: To obtain information on the causes of age-related bone loss in men and the concomitant decline in calcium absorption. Design: Cross-sectional study. Setting: Adelaide, South Australia, Australia. Subjects: A total of 95 healthy, Caucasian men (age range 27-87 y). Results: Calcium absorption declined with age (r ¼ À0.46, Po0.0001), as did 24-h urine calcium, phosphate and creatinine (r4À0.21, Po0.05 for all); serum calcitriol and 25 hydroxyvitamin D did not change with age. Calcium absorption was related to serum calcitriol (r ¼ 0.20, P ¼ 0.05). An inverse relation between the residual deviations in calcium absorption, after allowing for its dependence on calcitriol, and age (F ¼ 5.4, Po0.005) was observed. The 24-h urinary calcium, phosphate and creatinine were all related to calcium absorption (r40.41, Po0.0001). Forearm bone density fell with age (r ¼ À0.45, Po0.0001) but was not related to calcium absorption, or markers of bone turnover. Conclusions: In healthy Caucasian males (i) calcium absorption falls, but serum calcitriol does not change with age, (ii) the relation between calcium absorption and serum calcitriol changes with age, indicative of an intestinal resistance to calcitriol and (iii) calcium absorption is a significant determinant of 24-h urinary calcium excretion.

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Section: Discussionsupporting

confidence: 90%

“…Concomitant with the age-related decline in bone density in men, there is a fall in intestinal calcium absorption efficiency (Bullamore et al, 1970;Gallagher et al, 1979;Francis et al, 1989;Agnusdei et al, 1998). The latter accounts for some 50 % of the variance of calcium balance in postmenopausal women (Nordin & Morris, 1992).…”

Section: Introductionmentioning

confidence: 99%

Relation between calcium absorption and serum calcitriol in normal men: evidence for age-related intestinal resistance to calcitriol

et al. 2004

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“…Because intestinal calcium absorption decline with age in humans (Avioli et al 1965, Bullamore et al 1970 and rats (Russell et al 1986), a commonly held hypothesis suggests that this decreased absorption results from a sequence of events initiated by low estrogen levels, which result in bone resorption. According to this hypothesis, the released calcium increases the calcium concentration in extracellular spaces, thus suppressing parathyroid hormone secretion, a decrease in 1,25(OH) 2 D 3 production and plasma concentration follows, finally resulting in decreased intestinal calcium absorption (Gallagher et al 1979).…”

Section: Introductionmentioning

confidence: 99%

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Gilad

Bresler²,

J³

et al. 2005

Journal of Endocrinology

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We previously demonstrated that 17 -estradiol (E2) regulates the transcription and expression of the vitamin D receptor (VDR) in rat colonocytes and duodenocytes in vivo. The aim of the present study was to assess whether the extracellular signal-regulated kinase (ERK) induced by E2 is involved in regulating VDR expression. We compared E2-associated signaling activity in HT29 colon cancer cells, a non-classical E2-target, with that in MCF-7 breast cancer cells, the natural targets of the hormone. E2 did not affect proliferation of HT29 cells, but enhanced proliferation of MCF-7 cells. Vitamin D inhibited proliferation of both cell lines and the combined treatment induced potentiation of vitamin D activity. E2 upregulated VDR transcription and protein expression concomitantly with ERK 1/2 phosphorylation in both cell lines. PD98059, a specific mitogen-activated protein kinase (MAPK) inhibitor, prevented E2-mediated activation of ERK 1/2, with concomitant inhibition of VDR expression. ICI182780 inhibited VDR expression in HT29 and MCF-7 cell lines. A conjugate of E2 and bovine serum albumin upregulated phosphorylation of ERK 1/2 and concomitantly enhanced VDR expression in a similar fashion as the nonconjugated hormone. Expression of ER and ER was detected in MCF-7 and HT29 cell lines respectively, which localized to the nuclei, cytosol and caveolar membrane rather than non-caveolar membrane. Disruption of lipid rafts/caveolae by depleting cellular cholesterol with the cholesterol-binding reagentmethylcyclodextrin blocked ERK 1/2 phosphorylation concomitantly with VDR upregulation. The tyrosine phosphorylation inhibitor suramin and src kinase inhibitor PP2 inhibited both ERK 1/2 phosphorylation and VDR expression. E2 induced phosphorylation of Raf and Jun in a time-dependent manner. The Ras/Raf dependent inhibitor of transactivation sulindac sulfide also blocked E2 effects. The specific c-Jun phosphorylation inhibitor SP600125 dose dependently inhibited c-Jun phosphorylation and VDR expression. The MAPK/ERK kinase inhibitor PD 98059 downregulated both c-Jun phosphorylation and VDR expression indicating that upstream and downstream events in the signaling cascade are all related to the control of VDR expression. Taken together, our data suggest that E2 binds to receptors compartmentalized to membranal caveolar domains in HT29 and MCF-7 cells, inducing ERK 1/2 activation and transcriptional activity, which finally results in upregulation of expression of the VDR gene.

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“…There is an age related decrease in calcium absorption that contributes to further negative calcium balance (5,6). Malabsorption of calcium causes secondary hyperparathyroidism that increases bone resorption causing further bone loss.…”

Section: Age Related Changes In Calcium and Vitamin D Metabolismmentioning

confidence: 99%

Prevention and treatment of postmenopausal osteoporosis

J¹

1995

Clin Rheumatol

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In the beginning, that is from the 1960's, when a link between menopause and osteoporosis was first identified; estrogen treatment was the standard for preventing bone loss, however there was no fracture data, even though it was thought to be effective. This continued until the Women's Health Initiative (WHI) study in 2001 that published data on 6 years of treatment with hormone therapy that showed an increase in heart attacks and breast cancer. Even though the risks were small, 1 per 1500 users annually, patients were worried and there was a large drop off in estrogen use. In later analyses the WHI study showed that estrogen reduced fractures and actually prevented heart attacks in the 50-60 year age group. Estrogen alone appeared to be safer to use than estrogen + the progestin medroxyprogesterone acetate and actually reduced breast cancer.At the same time other drugs were being developed for bone that belong to the bisphosphonate group and the first generation of compounds showed moderate potency on bone resorption. The second and third generation compounds were much more potent and in a series of large trials were shown to reduce fractures. For the last 15 years the treatment of osteoporosis belonged to the bisphosphonate compounds, most of which reduce fracture rates by 50 percent. With the exception of gastrointestinal irritation the drugs are well tolerated and highly effective. The sophistication of the delivery systems now allow treatment that can be given daily, weekly, monthly and annually either orally or intravenously Bone remodeling is a dynamic process that repairs microfractures and replaces old bone with new bone. In the last 10 years there has been a remarkable understanding of bone biology so that new therapies can be specifically designed on a biological basis. The realization that RANKL was the final cytokine involved in the resorption process and that marrow cells produced a natural antagonist called Osteoprotegerin (OPG) quickly led to two lines of therapy. First OPG was used as a therapy to block RANKL was initially successful © 2013 Elsevier Ltd. All rights reserved. * Corresponding author Phone: 402-280-4518 Fax: 402-280-4517 jcg@creighton.edu.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript but later antibodies against OPG developed and this line of treatment had to be discontinued. The next step was to develop a monoclonal antibody against RANKL and this proved to be highly effective in blocking bone resorption. It led to development of a drug De...

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Effect of Age on Calcium Absorption

Cited by 410 publications

References 7 publications

Relation between calcium absorption and serum calcitriol in normal men: evidence for age-related intestinal resistance to calcitriol

Relation between calcium absorption and serum calcitriol in normal men: evidence for age-related intestinal resistance to calcitriol

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Prevention and treatment of postmenopausal osteoporosis

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