Acquired alterations in vitamin D metabolism in the acidotic state

Baran, Daniel T.; Lee, Sook Won; Jo, Oak D.; Avioli, Louis V.

doi:10.1007/bf02411228

Cited by 26 publications

(4 citation statements)

References 30 publications

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“…2). Our finding of an enhanced 1,25-(OH)2D MCR represents the first report ofthis measurement in acidosis and is consistent with recent results ofstudies demonstrating enhanced degradation of labeled 1,25-(OH)2D in vitamin D-deficient chicks with NH4Cl-induced metabolic acidosis (33). The mechanism of the apparent acidosis-induced enhancement of MCR has not been investigated in this study.…”

Section: Resultssupporting

confidence: 92%

Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia.

Krapf¹,

Vetsch²,

W³

et al. 1992

J. Clin. Invest.

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IntroductionChronic metabolic acidosis results in metabolic bone disease, calcium nephrolithiasis, and growth retardation. The pathogenesis of each of these sequelae is poorly understood in humans. We therefore investigated the effects ofchronic extrarenal metabolic acidosis on the regulation of 1,25-(OH)2D, parathyroid hormone, calcium, and phosphate metabolism in normal humans. Chronic extrarenal metabolic acidosis was induced by administering two different doses of NH4CI 12.1 (low dose) and impaired conversion of 25-(OH)D to 1,25-(OH)2D ( 15).However, the results of measurements of serum 1,25-(OH)2D concentration during experimentally induced metabolic acidosis have not been consistent: reported values have ranged from increased to unchanged to decreased mean concentrations (15)(16)(17)(18)(19). These inconsistencies may have been due in part to the experimental difficulties in controlling acidosisinduced alterations in the plasma concentrations of known modulators of 1,25-(OH)2D production: phosphate (20-22), calcium (23), and parathyroid hormone (23,24

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Section: Resultssupporting

confidence: 92%

Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia.

Krapf¹,

Vetsch²,

W³

et al. 1992

J. Clin. Invest.

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“…Acidosis inhibits the production of 1,25(OHhD 3 by suppressing renal I-a-hydroxylase activity in chicks and rats raised on vitamin D-deficient diets and supplied with exogenous vitamin D 3 (20)(21)(22)(23)(24)(25), however, this suppression of hydroxylase activity is attenuated with prolonged acidosis (26). In vitamin D-replete rats, serum 1,25(OHhD 3 Ievels are either normal or elevated and rise in response to calcium and phosphate restriction (27,28).…”

Section: Effect Of 125(ohhd 3 On Phosphate Uptake Into Bbmv From Acimentioning

confidence: 99%

The Effects of Metabolic Acidosis on Jejunal Phosphate and Glucose Transport in Weanling Rats

Borowitz

Said

1986

Pediatr Res

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MATERIALS AND METHODSStudy design. Newborn litters of Sprague Dawley rats were obtained from Sasco Industries (Omaha, NE). Mothers were allowed free access to food and water, and the pups were allowed to suckle freely. At 17 days of age, litters were separated from the mothers and randomly divided into two groups. Group I (acidotic) was offered pulverized standard food to eat and 1.5% NH 4 Cl to drink. The animals were allowed free access to water and food. Group 2 (control) was pair fed as a group with the first group and offered water to drink ad libitum. After 3 days, arterial blood gases were obtained, and jejunal glucose and phosphate transport were measured in vivo and in vitro.In vivo transport studies. In vivo transport was measured using a recirculating perfusion technique (II). Briefly, the proximal 20 cm of jejunum were cannulated with polyethylene inflow and outflow catheters and flushed with ice cold saline buffer and air. The intestinal segment was perfused at 0.1 ml/min with a solution consisting of 145 mM NaCl, 20 mM Hepes/Tris (pH 6.5), and 0.1 mM glucose labelled with 3H-glucose (specific activity 50 Cijmmol, New England Nuclear, Boston, MA), or 0.3 mM KH 2 P04 labeled with KHPP04 (specific activity 1 Cijmmol, New England Nuclear). After a 20-min equilibration period, duplicate 100-tLl aliquots were sampled every 10 min for 40 min. The rate of glucose or phosphate absorption was calculated by determining the rate of disappearance of the solute from the perfusate. Fluid shifts were assessed using 3H or 14C labeled inulin as a nonabsorable marker (specific activity 0.5 and 50 Cijmol, respectively, New England Nuclear) and absorption was corrected for fluid shifts. 3H, 14C, and 32P-labeled radioactivities were determined by double isotope counting and calculating techniques (12). Absorption results were expressed in terms of dry intestinal length since dry length correlates best with intestinal surface area (13).In vitro transport studies. In vitro transport was measured using jejunal brush border membrane vesicles (14). Briefly, animals were anesthetized with ether and 0.4 ml of blood was withdrawn from the abdominal aorta for arterial blood gas measurements. The entire jejunum was removed and washed with ice cold 0.9 N saline and everted over a glass rod. Brush border membrane vesicles were prepared by sequential precipitation with 0.01 M MgCb and differential centrifugation (15). The purity of the vesicle preparation for rats of varying ages has been previously demonstrated in our laboratory using morphologic criteria, enzymatic enrichment studies, and functional transport studies (15).Glucose and phosphate uptakes were measured by a rapid filtration technique (16) using Sartorius cellulose nitrate filters of 0.45 tLm pore size (Sartorius Filters Inc., Hayward, CA) that had been presoaked in stop solution containing 100 mM mannitol, 100 mM choline chloride, 20 mM hepes/tris, and 50 mM magnesium chloride (pH 7.4). Glucose stop solution also con-763ABSTRACf. To investigate the effects of metaboli...

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“…It is not clear, at the moment, whether the defect in l,25(OH)2D3 produc tion is secondary to the metabolic acidosis [85][86][87] or whether it is also a primary tubular defect. Interestingly, as in patients with X-linked dominant hypophospha témie rickets, despite the clinical manifestations of rick ets and the low serum l,25(OH)2D3 concentration, serum PTH concentration is usually normal.…”

Section: Type 2 -Proximal Renal Tubular Acidosismentioning

confidence: 99%

“…In distal RTA, the difference will be less than 20 mm Hg, whereas in proximal RTA the difference will be more than 20 mm Hg. The method is useful particularly for the detection of cases with incomplete distal RTA in which the acidification defect is exposed only under challenge [87,115].…”

Section: Principles Of Laboratory Workup Of Rta Typesmentioning

confidence: 99%