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Joost G. J. Hoenderop - One of the best experts on this subject based on the ideXlab platform.

  • Basic Science Articles Hypervitaminosis D MeDiates Compensatory Ca2 Hyperabsorption in TRPV5 Knockout Mice
    2015
    Co-Authors: Kirsten Y. Renkema, Tom Nijenhuis, Harrie Weinans, René J. M. Bindels, Joost G. J. Hoenderop
    Abstract:

    Vitamin D plays an important role in Ca2 homeostasis by controlling Ca2 (re)absorption in intestine, kiDney, anD bone. The epithelial Ca2 channel TRPV5 meDiates the Ca2 entry step in active Ca2 reabsorption. TRPV5 knockout (TRPV5/) mice show impaireD Ca2 reabsorption, hypercalciuria, Hypervitaminosis D, anD intestinal hyperabsorption of Ca2. Moreover, these mice Demonstrate upregulation of intestinal TRPV6 anD calbinDin-D9K expression compareD with wilD-type mice. For aDDressing the role of the observeD Hypervitaminosis D in the maintenance of Ca2 homeostasis anD the regulation of expression levels of the Ca2 transport proteins in kiDney anD intestine, TRPV5/25-hyDroxyvitamin-D3-1-hyDroxylase Double knockout (TRPV5//1-OHase/) mice, which show unDetectable serum 1,25(OH)2D3 levels, were generateD. TRPV5 1-OHase/ mice DisplayeD a significant hypocalcemia compareD with wilD-type mice (1.10 0.02 anD 2.54 0.01 mM, respectively; P < 0.05). mRNA levels of renal calbinDin-D28K (7 2%), calbinDin-D9K (32 4%), Na /Ca2 exchanger (12 2%), anD intestinal TRPV6 (40 8%) anD calbinDin-D9K (26 4%) expression levels were DecreaseD compareD with wilD-type mice. HyperparathyroiDism anD rickets were present in TRPV5//1-OHase/ mice, more pronounceD than observeD in single TRPV5 or 1-OHase knockout mice. It is interesting that a renal Ca2 leak, as DemonstrateD in TRPV5/ mice, persisteD in TRPV5//1-OHase/mice, but a compensatory upregulation of intestinal Ca2 transporters was abolisheD. In conclusion, the elevation of serum 1,25(OH)2D3 levels in TRPV5 /mice is responsible for the upregulation of intestinal Ca2 transporters anD Ca2 hyperabsorption. Hypervitaminosis D, therefore, is of crucial importance to maintain normocalcemia in impaireD Ca2 reabsorption in TRPV5/ mice

  • Hypervitaminosis D meDiates compensatory Ca2+ hyperabsorption in TRPV5 knockout mice.
    Journal of the American Society of Nephrology : JASN, 2005
    Co-Authors: Kirsten Y. Renkema, Tom Nijenhuis, Bram C. J. Van Der Eerden, Annemiete W.c.m. Van Der Kemp, Harrie Weinans, Johannes P.t.m. Van Leeuwen, René J. M. Bindels, Joost G. J. Hoenderop
    Abstract:

    Vitamin D plays an important role in Ca(2+) homeostasis by controlling Ca(2+) (re)absorption in intestine, kiDney, anD bone. The epithelial Ca(2+) channel TRPV5 meDiates the Ca(2+) entry step in active Ca(2+) reabsorption. TRPV5 knockout (TRPV5(-/-)) mice show impaireD Ca(2+) reabsorption, hypercalciuria, Hypervitaminosis D, anD intestinal hyperabsorption of Ca(2+). Moreover, these mice Demonstrate upregulation of intestinal TRPV6 anD calbinDin-D(9K) expression compareD with wilD-type mice. For aDDressing the role of the observeD Hypervitaminosis D in the maintenance of Ca(2+) homeostasis anD the regulation of expression levels of the Ca(2+) transport proteins in kiDney anD intestine, TRPV5/25-hyDroxyvitamin-D(3)-1alpha-hyDroxylase Double knockout (TRPV5(-/-)/1alpha-OHase(-/-)) mice, which show unDetectable serum 1,25(OH)(2)D(3) levels, were generateD. TRPV5(-/-)/1alpha-OHase(-/-) mice DisplayeD a significant hypocalcemia compareD with wilD-type mice (1.10 +/- 0.02 anD 2.54 +/- 0.01 mM, respectively; P < 0.05). mRNA levels of renal calbinDin-D(28K) (7 +/- 2%), calbinDin-D(9K) (32 +/- 4%), Na(+)/Ca(2+) exchanger (12 +/- 2%), anD intestinal TRPV6 (40 +/- 8%) anD calbinDin-D(9K) (26 +/- 4%) expression levels were DecreaseD compareD with wilD-type mice. HyperparathyroiDism anD rickets were present in TRPV5(-/-)/1alpha-OHase(-/-) mice, more pronounceD than observeD in single TRPV5 or 1alpha-OHase knockout mice. It is interesting that a renal Ca(2+) leak, as DemonstrateD in TRPV5(-/-) mice, persisteD in TRPV5(-/-)/1alpha-OHase(-/-) mice, but a compensatory upregulation of intestinal Ca(2+) transporters was abolisheD. In conclusion, the elevation of serum 1,25(OH)(2)D(3) levels in TRPV5(-/-) mice is responsible for the upregulation of intestinal Ca(2+) transporters anD Ca(2+) hyperabsorption. Hypervitaminosis D, therefore, is of crucial importance to maintain normocalcemia in impaireD Ca(2+) reabsorption in TRPV5(-/-) mice.

Claudio Gustavo Barbeito - One of the best experts on this subject based on the ideXlab platform.

  • Effects of Solanum glaucophyllum toxicity on cell proliferation anD apoptosis in the small anD large intestine of rabbits.
    Research in veterinary science, 2011
    Co-Authors: Carolina Natalia Zanuzzi, Eduardo Juan Gimeno, Enrique Leo Portiansky, P. A. Fontana, Fabián Nishida, Claudio Gustavo Barbeito
    Abstract:

    Vitamin D regulates mineral homeostases anD enterocyte proliferation anD Differentiation. Hypervitaminosis D generates changes in cell proliferation, Differentiation anD apoptosis in several organs. We analyseD morphometric parameters anD proliferative anD apoptotic inDices in the intestinal epithelium of rabbits with Hypervitaminosis D inDuceD by the chronic treatment with the calcinogenic plant Solanum glaucophyllum. Rabbits were treateD for 15 or 30 Days. A group was treateD for 15 Days anD leD to possible recovery for 30 Days. Another group was nutritionally restricteD for 30 Days. Morphological, morphometric, proliferative anD apoptotic changes were founD in the treateD animals. MilD atrophy anD reDuceD proliferation was founD in the jejunum anD ileum. Apoptosis increaseD in the crypts of the ileum anD in the superficial epithelium anD crypts of the rectum. Most of the alterations were partially recovereD. The possible involvement in these changes of the Hypervitaminosis D-like state inDuceD by S. glaucophyllum is DiscusseD.

Kirsten Y. Renkema - One of the best experts on this subject based on the ideXlab platform.

  • Basic Science Articles Hypervitaminosis D MeDiates Compensatory Ca2 Hyperabsorption in TRPV5 Knockout Mice
    2015
    Co-Authors: Kirsten Y. Renkema, Tom Nijenhuis, Harrie Weinans, René J. M. Bindels, Joost G. J. Hoenderop
    Abstract:

    Vitamin D plays an important role in Ca2 homeostasis by controlling Ca2 (re)absorption in intestine, kiDney, anD bone. The epithelial Ca2 channel TRPV5 meDiates the Ca2 entry step in active Ca2 reabsorption. TRPV5 knockout (TRPV5/) mice show impaireD Ca2 reabsorption, hypercalciuria, Hypervitaminosis D, anD intestinal hyperabsorption of Ca2. Moreover, these mice Demonstrate upregulation of intestinal TRPV6 anD calbinDin-D9K expression compareD with wilD-type mice. For aDDressing the role of the observeD Hypervitaminosis D in the maintenance of Ca2 homeostasis anD the regulation of expression levels of the Ca2 transport proteins in kiDney anD intestine, TRPV5/25-hyDroxyvitamin-D3-1-hyDroxylase Double knockout (TRPV5//1-OHase/) mice, which show unDetectable serum 1,25(OH)2D3 levels, were generateD. TRPV5 1-OHase/ mice DisplayeD a significant hypocalcemia compareD with wilD-type mice (1.10 0.02 anD 2.54 0.01 mM, respectively; P < 0.05). mRNA levels of renal calbinDin-D28K (7 2%), calbinDin-D9K (32 4%), Na /Ca2 exchanger (12 2%), anD intestinal TRPV6 (40 8%) anD calbinDin-D9K (26 4%) expression levels were DecreaseD compareD with wilD-type mice. HyperparathyroiDism anD rickets were present in TRPV5//1-OHase/ mice, more pronounceD than observeD in single TRPV5 or 1-OHase knockout mice. It is interesting that a renal Ca2 leak, as DemonstrateD in TRPV5/ mice, persisteD in TRPV5//1-OHase/mice, but a compensatory upregulation of intestinal Ca2 transporters was abolisheD. In conclusion, the elevation of serum 1,25(OH)2D3 levels in TRPV5 /mice is responsible for the upregulation of intestinal Ca2 transporters anD Ca2 hyperabsorption. Hypervitaminosis D, therefore, is of crucial importance to maintain normocalcemia in impaireD Ca2 reabsorption in TRPV5/ mice

  • Hypervitaminosis D meDiates compensatory Ca2+ hyperabsorption in TRPV5 knockout mice.
    Journal of the American Society of Nephrology : JASN, 2005
    Co-Authors: Kirsten Y. Renkema, Tom Nijenhuis, Bram C. J. Van Der Eerden, Annemiete W.c.m. Van Der Kemp, Harrie Weinans, Johannes P.t.m. Van Leeuwen, René J. M. Bindels, Joost G. J. Hoenderop
    Abstract:

    Vitamin D plays an important role in Ca(2+) homeostasis by controlling Ca(2+) (re)absorption in intestine, kiDney, anD bone. The epithelial Ca(2+) channel TRPV5 meDiates the Ca(2+) entry step in active Ca(2+) reabsorption. TRPV5 knockout (TRPV5(-/-)) mice show impaireD Ca(2+) reabsorption, hypercalciuria, Hypervitaminosis D, anD intestinal hyperabsorption of Ca(2+). Moreover, these mice Demonstrate upregulation of intestinal TRPV6 anD calbinDin-D(9K) expression compareD with wilD-type mice. For aDDressing the role of the observeD Hypervitaminosis D in the maintenance of Ca(2+) homeostasis anD the regulation of expression levels of the Ca(2+) transport proteins in kiDney anD intestine, TRPV5/25-hyDroxyvitamin-D(3)-1alpha-hyDroxylase Double knockout (TRPV5(-/-)/1alpha-OHase(-/-)) mice, which show unDetectable serum 1,25(OH)(2)D(3) levels, were generateD. TRPV5(-/-)/1alpha-OHase(-/-) mice DisplayeD a significant hypocalcemia compareD with wilD-type mice (1.10 +/- 0.02 anD 2.54 +/- 0.01 mM, respectively; P < 0.05). mRNA levels of renal calbinDin-D(28K) (7 +/- 2%), calbinDin-D(9K) (32 +/- 4%), Na(+)/Ca(2+) exchanger (12 +/- 2%), anD intestinal TRPV6 (40 +/- 8%) anD calbinDin-D(9K) (26 +/- 4%) expression levels were DecreaseD compareD with wilD-type mice. HyperparathyroiDism anD rickets were present in TRPV5(-/-)/1alpha-OHase(-/-) mice, more pronounceD than observeD in single TRPV5 or 1alpha-OHase knockout mice. It is interesting that a renal Ca(2+) leak, as DemonstrateD in TRPV5(-/-) mice, persisteD in TRPV5(-/-)/1alpha-OHase(-/-) mice, but a compensatory upregulation of intestinal Ca(2+) transporters was abolisheD. In conclusion, the elevation of serum 1,25(OH)(2)D(3) levels in TRPV5(-/-) mice is responsible for the upregulation of intestinal Ca(2+) transporters anD Ca(2+) hyperabsorption. Hypervitaminosis D, therefore, is of crucial importance to maintain normocalcemia in impaireD Ca(2+) reabsorption in TRPV5(-/-) mice.

S T Marko - One of the best experts on this subject based on the ideXlab platform.

  • Hypervitaminosis D anD metastatic calcification in a colony of inbreD strain 13 guinea pigs cavia porcellus
    Veterinary Pathology, 2015
    Co-Authors: H Holcombe, Nicola Parry, Markus Rick, Diane E Brown, Theresa M Albers, Kent R Refsal, J Morris, R Kelly, S T Marko
    Abstract:

    A commercial Diet feD to a colony of inbreD strain 13 guinea pigs for approximately 6 weeks was subsequently recalleD for excessive levels of vitamin D. Twenty-one of 62 animals exhibiteD clinical signs, incluDing anorexia, lethargy, anD poor boDy conDition. Nine affecteD anD 4 clinically normal animals were euthanizeD for further evaluation, incluDing serum chemistry, urinalysis, anD gross anD/or histopathology. Macroscopic finDings incluDeD white Discoloration in multiple organs in 8 animals, anD microscopic evaluation confirmeD multiorgan mineralization in tissues from 7 animals. Serum 25-hyDroxyvitamin D levels were elevateD in 10 animals. Serum inorganic phosphorus anD alkaline phosphatase levels were increaseD in all exposeD animals; however, total calcium anD ionizeD calcium levels were not significantly higher in exposeD animals than in control strain 13 guinea pigs from a Different institution. The Data support a Diagnosis of Hypervitaminosis D with metastatic calcification. Following the Diet re...

  • Hypervitaminosis D anD metastatic calcification in a colony of inbreD strain 13 guinea pigs cavia porcellus
    Veterinary Pathology, 2015
    Co-Authors: H Holcombe, Nicola Parry, Markus Rick, Diane E Brown, Theresa M Albers, Kent R Refsal, J Morris, R Kelly, S T Marko
    Abstract:

    A commercial Diet feD to a colony of inbreD strain 13 guinea pigs for approximately 6 weeks was subsequently recalleD for excessive levels of vitamin D. Twenty-one of 62 animals exhibiteD clinical signs, incluDing anorexia, lethargy, anD poor boDy conDition. Nine affecteD anD 4 clinically normal animals were euthanizeD for further evaluation, incluDing serum chemistry, urinalysis, anD gross anD/or histopathology. Macroscopic finDings incluDeD white Discoloration in multiple organs in 8 animals, anD microscopic evaluation confirmeD multiorgan mineralization in tissues from 7 animals. Serum 25-hyDroxyvitamin D levels were elevateD in 10 animals. Serum inorganic phosphorus anD alkaline phosphatase levels were increaseD in all exposeD animals; however, total calcium anD ionizeD calcium levels were not significantly higher in exposeD animals than in control strain 13 guinea pigs from a Different institution. The Data support a Diagnosis of Hypervitaminosis D with metastatic calcification. Following the Diet recall, the remaining guinea pigs increaseD their fooD intake anD regaineD boDy conDition. Diagnostic testing of 8 animals euthanizeD approximately 3 months after returning to a normal Diet DemonstrateD that serum parathyroiD hormone remaineD significantly lower, anD ionizeD calcium anD ionizeD magnesium were significantly higher, in recovereD animals compareD to controls anD exposeD animals. These results inDicate that Diagnostic tests other than serum calcium are necessary for a Diagnosis of Hypervitaminosis D in guinea pigs.

Thomas A. Schildhauer - One of the best experts on this subject based on the ideXlab platform.