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Vitamin D status

In summary, the results of this life-long experiment on female mice indicated that low or high Ca intake early in life did not have any significant effect on the skeletal Ca in adulthood, but the continued high Ca intake reduced the turnover rate in old age. Consequently the strengh of the bone was better preserved than that in the mice fed the low Ca diet. This supports the use of Ca supplements even in old patients suffering from osteoporosis, provided their vitamin D status is adequate. Dietary fluoride... [Pg.152]

The principal circulating form of vitamin D is 25-hydroxy vitamin D and it is this form of the vitamin that is measured in efforts to determine your vitamin D status. [Pg.199]

Willett AM. Vitamin D status and its relationship with parathyroid hormone and bone mineral status in older adolescents. Proc Nutr Soc. 2005 64 193-203. [Pg.475]

The circulating levels of l,25(OH)2D3 rise progressively towards the end of pregnancy, probably in response to the increased mineral demands. At the same time, an extra-renal synthesis of l,25(OH)2D3 takes place in the fetoplacental unit [4,47,48]. This synthesis is thought to occur in the decidual cells rather than in the placenta itself, although some controversy still remains upon the exact location of this process. Placental tissues have also been shown to contain specific receptors for l,25(OH)2D3 [49] as well as the faculty to synthesize the small calbindin (9 kDa) [50], However, the transplacental calcium transport is independent of the overall maternal vitamin D status [51]. The hypothesis of a differential regulation of calcium transport within the feto/placental unit may be in relation with the in situ synthesis of l,25(OH)2D3 or the fetal synthesis of this hormone. [Pg.279]

Vitamin D that is taken up by the fiver is converted to 25-hydroxyvitamin D by a microsomal hydroxylase (Fig. 30-3). 25-Hydroxyvitamin D is the main circulating form of vitamin D in the serum and the best indicator of vitamin D status. Normal serum levels are 14-60 ng/mL (35-150 nmol/L). When serum calcium concentrations decline, 25-hydroxyvitamin D is converted to 1,25-dihydroxyvitmin D by la-hydroxylase, a mixed-function oxidase that is located in the inner mitochondrial membrane in kidney tissue and whose expression is regulated by parathyroid hormone (PTH). The main function of 1,25-dihydroxyvitamin D is to increase the intestinal absorption of dietary calcium and phosphorus. When serum concentrations of calcium and phosphorus are normal or when large doses of vitamin D are administered, 25-hydroxyvitamin D is metabolized to 24,25-dihydroxyvitamin D in the renal... [Pg.328]

Adipocytes have vitamin D receptors, and there is evidence that vitamin D may act as a suppressor of adipocyte development (Kawada et al., 1996). It has been suggested that vitamin D inadequacy may be a factor in the development of the metabolic syndrome ( syndrome X, the combination of insulin resistance, hyperlipidemia, and atherosclerosis associated with abdominal obesity). Sunlight exposure, and hence vitamin D status, may be a factor in the difference in incidence of atherosclerosis and myocardial infarction between northern and southern European countries in addition to effects on adipocyte development, calcitriol also enhances insulin secretion through induction of calbindin-D (Section 3.3.7.1), and there is some evidence vitamin D supplements can improve glucose tolerance (Boucher, 1998). [Pg.97]

Osteomalacia is the defective remineralization of bone during normal bone turnover in adults, so that there is a progressive demineralization, but with adequate bone matrix, leading to bone pain and skeletal deformities, with muscle weakness. Women with inadequate vitamin D status are especially at risk of osteomalacia after repeated pregnancies, as a result of the considerable drain on calcium reserves for fetal bone mineralization and lactation. [Pg.99]

Osteocalcin is induced in osteoblasts by calcitriol, and circulating osteocalcin can be used as an index of calcitriol action and metabolic bone disease. In rachitic children, the plasma concentration of osteocalcin is lower than in controls, and rises on therapy, remaining high until there is radiological evidence of cure. However, plasma osteocalcin can be undetectably low in normal subjects with adequate vitamin D status, so this does not provide a useful indication of deficiency (Greig et al., 1989). [Pg.103]

The plasma concentration of calcidiol is the most sensitive and usefiil index of vitamin D status, and is correlated with elevated plasma parathyroid hormone and alkaline phosphatase activity (Table 3.4). As shown in Table 3.2, the reference range of plasma calcidiol is between 20 to 150 nmol per L, with a twofold seasonal variation in temperate regions. Concentrations below 20 nmol per L are considered to indicate impending deficiency, and osteomalacia is seen in adults when plasma calcidiol falls below 10 nmol per L. In children, clinical signs of rickets are seen when plasma calcidiol faUs below 20 nmol per L. The plasma concentration of calcitriol does not give a useful indication of vitamin D status. The reference range is between 38 to 144 pmol per L and is maintained because of the stimulation of calcidiol 1-hydroxylation by parathyroid hormone secreted in response to faUing concentrations of calcium (Holick, 1990). [Pg.103]

Boucher BJ (1998) Inadequate vitamin D status does it contribute to the disorders comprising syndrome X British Journal of Nutrition 79, 315-27. [Pg.415]

Cholestasis-linked osteopathy (M. Loeper et al., 1939), which occurs much more frequently in the form of osteoporosis than osteomalacia, can be expected in up to 50% of cases. The pathogenesis is complex. Vitamin D status can be examined by determining 25-OH-cholecal-ciferol in the serum. Intestinal calcium loss and reduced calcium absorption due to vitamin D deficiency are key pathogenetic factors. It is still a matter of debate whether vitamin K deficiency (which can lead to reduced osteocalcin synthesis) and deficiencies in IGF I and II (which can cause dysfunction of the osteoblasts) are possible causes of this condition. Muscle and bone pain are frequent clinical symptoms, occurring mainly in the wrists and ankles. [Pg.240]

Determination of vitamin D is useful in the differential diagnosis of hypocalcemia, hypercalcemia, or hypercalciuria and for evaluating vitamin D status in health and in bone and mineral disorders (see Calcium, Clinical Significance, Hypocalcemia, and Hypercalcemia and Metabolic Bone Diseases). Only the measurements of 25(OH)D and 1,25(0H)2D have proven clinical value. Routine cfinical determination of vitamin D, 24,25(0H)2D, or other metabolites is not indicated at this time. [Pg.1922]

Radioimmunoassay. Before the development of the method described below, RIAs were not widely used in the United States because previous antisera (1) did not reliably measure vitamin D status, since they discriminated between l,25(OH)2D2 and l,25(OH)2D3, and (2) cross-reacted with other vitamin D metabolites to a much greater extent than VDR requiring more extensive sample purification, includ-ing preparative hPLC. " ... [Pg.1924]

Hollis BW, Kamerud JQ, Selvaag SR, Lorenz JD, Napoli JL. Determination of vitamin D status by radioimmunoassay with an l-Iabeled tracer, Clin Chem 1993 39 529-33. [Pg.1953]

Hoihs BW, Napoli JL. Improved radioimmunoassay for vitamin D and its use in assessing vitamin D status. Clin Chem 1985 31 1815-9. [Pg.1953]

Sherman SS, Hollis BW, Tobin JD. Vitamin D status and related parameters in a healthy population the effects of age, sex and season. J Clin Endocrinol Metab 1990 71 405-13. [Pg.1962]

SouberbieUe JC, Cormier C, Kindermans C, Gao P, Cantor T, Forette F, Baulieu EE. Vitamin D status and... [Pg.1962]


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See also in sourсe #XX -- [ Pg.197 , Pg.198 , Pg.201 ]




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Vitamin status

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