Vitamin D and Growth1

Steenbock, H.; Herting, David C.

doi:10.1093/jn/57.4.449

Cited by 169 publications

(51 citation statements)

References 31 publications

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“…The concentrations of vitamin D3 in serum were in good agreement with those obtained by Jones8 and by Shepard et al 9, although the values were slightly lower than those given by Aksnes10 and Seamark et al '5 The mean value of 25-OHD3 obtained by this study was similar to those reported by other workers.l- 22 The concentrations of the vitamins in normal rat serum determined by the method are shown in Table 4. The levels of the vitamins in rat serum were ca.…”

Section: Determination Of Vitamin D3 and 25-ohd3 In Serumsupporting

confidence: 90%

Determination of Vitamin D3 and 25-Hydroxyvitamin D3 in Sera by Column-Switching High Performance Liquid Chromatography with Fluorescence Detection

et al. 1990

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A column-switching high performance liquid chromatographic method with fluorescence detection for the determination of vitamin D3 and 25-hydroxyvitamin D3 in human and rat sera is described. The vitamins in a lipid extract from serum, obtained by solid-phase extraction technique using a Bond-Slut C18 cartridge, are converted with 3,4-dihydro-6,7-dimethoxy-4-methyl-3-oxoquinoxaline-2-carbonyl azide into the corresponding fluorescent derivatives. The derivatives are separated from endogenous interfering substances by column-switching chromatography. The chromatographic system consisted of a precolumn chromatography for clean-up of the derivatives and an analytical column chromatography for the complete separation of the derivatives. The derivatives are detected fluorometrically at excitation and emission wavelengths of 360 and 440 nm, respectively. The detection limits (S/ N=3) for vitamin D3 and 25-hydroxyvitamin D3 are 15 and 8 fmol, respectively, in a 10 µl injection volume. The sensitivity permits simultaneous determination of the vitamins in 1 ml of normal human and rat sera. KeywordsVitamin D3, 25-hydroxyvitamin D3, column-switching high performance liquid chromatography, fluorescence detection, 3,4-dihydro-6,7-dimethoxy-4-methyl-3-oxoquinoxaline-2-carbonyl azide, human serum, rat serum Vitamin D3 is hydroxylated in the liver to 25-hydroxyvitamin D3 (25-OHD3), which is further hydroxylated in the kidney either to 1 a,25-dihydroxyvitamin D3 or to 24,25-dihydroxyvitamin D3. The determination of these compounds in human plasma/ serum is very important for the assessment of "vitamin D3 status" in healthy and diseased persons. Among these compounds, vitamin D3 and 25-OHD3 occur in serum at relatively high concentrations. Thus, their determination is still widely used for the assessment of vitamin D3 status and provides significant results in many clinical situations.Various methods for the determination of vitamin D3 and/ or 25-OHD3 in human plasma/ serum have been reported.l-22 The methods include lipid extraction, purification by chromatography and quantification by physicochemical methods such as UV-absorption'-14 and mass fragmentography15, competitive protein binding assaysg-14"7-22 or radioimmunoassay.14 Among these methods, the UV-high performance liquid chromatographic (HPLC) methods have been widely used for the simultaneous determination of vitamin D3 and 25-OHD3 in plasma/ serum. Such methods, however, include an extremely complicated pretreatment of plasma! serum, and require a very long time for the determination.We have developed 3,4-dihydro-6,7-dimethoxy-4-methyl-3-oxoquinoxaline-2-carbonyl azide (DMEQ-CONS) as a highly sensitive and reactive fluorescence derivatization reagent for alcohols.23 The reagent has then been applied to the determination of cholesterol and cholestanol in human serum24,25, and 7-dehydrocholesterol (previtamin D3) in rat26 and human skin surfaces.27 Recently, we found that vitamin D3 and 25-OHD3 react with DMEQ-CONS to give the corresponding highly fluorescent carbamic acid...

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Section: Determination Of Vitamin D3 and 25-ohd3 In Serumsupporting

confidence: 90%

Determination of Vitamin D3 and 25-Hydroxyvitamin D3 in Sera by Column-Switching High Performance Liquid Chromatography with Fluorescence Detection

et al. 1990

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“…(Underwood & DeLuca, 1984;Weinstein, Underwood, Hutson & DeLuca, 1984). Furthermore, dietary calcium and phosphorus have been shown to exert a major influence on body growth (Steenbock & Herting, 1955). The experimental strategy used in the present study was therefore aimed at controlling the secondary effects of vitamin D deprivation by maintaining vitamin-D-deficient rats normocalcaemic and euparathyroid through dietary supplementation with calcium.…”

Section: Salivary Calcium and Amylasementioning

confidence: 99%

Vitamin D and parotid gland function in the rat.

Peterfy

Tenenhouse

1988

The Journal of Physiology

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SUMMARY1. We previously reported that parotid gland secretion is decreased in rats deprived of vitamin D (Glijer, Peterfy & Tenenhouse, 1985). In the present study we examine whether this effect is a direct result of the absence of vitamin D or due to the secondary systemic effects of vitamin D deficiency.2. Offspring of rats maintained on a calcium-supplemented (1-2%), vitamin-Ddeficient diet were weaned onto the same diet and examined after 8 weeks. Using this method it was possible to maintain serum calcium and parathyroid hormone concentrations within normal limits. Serum 25-hydroxyvitamin D (25(OH)D3) was not detectable, but 1,25-dihydroxyvitamin D (1,25(OH)2D3) concentrations were normal.3. Pilocarpine-stimulated flow of parotid saliva was reduced 57 % in vitamin-Ddeprived animals, but amylase secretion was unchanged. Treatment with vitamin D3 returned flow rates to normal.4. The concentration of calcium in parotid saliva was normal in vitamin-Ddeprived rats, although total parotid calcium output was reduced 57 %.5. Pilocarpine-stimulated salivary flow from submandibular gland, a tissue which does not possess 1,25(OH)2D3 receptors, was normal in vitamin-D-deprived rats.6. Heart rate and arterial blood pressure changes in response to i.v. pilocarpine administration were identical in normal and vitamin-D-deficient rats.7. Auriculotemporal nerve-stimulated flow of parotid saliva was also reduced by 50% and administration of vitamin D3 to these rats corrected this abnormality.8. It is concluded that fluid and electrolyte secretion from parotid gland is directly dependent on vitamin D; abnormal parotid gland function seen in vitamin-Ddeficient rats is not due to secondary hypocalcaemia or hyperparathyroidism, nor can it be explained by haemodynamic changes evoked during systemic administration of pilocarpine. We further conclude that the metabolite of vitamin D responsible for this effect is not 1,25(OH)2D3.

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“…This substance is more active than vitamin D3 itself in curing rickets when administered in vivo and acts more rapidly in stimulating the intestinal absorption of calcium as well as mobilization of bone (3). Whereas it has never been possible to demonstrate a direct effect of small doses of vitamin D on bone or intestine, 25-hydroxycholecalciferol has proved to be directly active in vitro in trace amounts on bone resorption (4) and intestinal transport of calcium (5). These new evidences support the concept that 25-hydroxycholecalciferol may be the metabolically active form of vitamin D3.…”

Section: Introductionmentioning

confidence: 99%

“…It has been possible to show that the liver is responsible for this transient increase in plasma radioactivity by quickly releasing into the blood a large porReceived for publication 25 February 1969 and in revised form 22 May 1969. tion of the dose which had been initially cleared from the plasma and accumulated in the liver. At the very same time, 25-hydroxycholecalciferol starts to accumulate in the plasma and in the tissues (7). These observations led us to postulate the liver as the site of hydroxylation of vitamin D3 into its active metabolite, 25-hydroxycholecalciferol.…”

Section: Introductionmentioning

confidence: 99%