Molecular aspects of intestinal calcium absorption
- Autores
- Díaz de Barboza, Gabriela; Guizzardi, Solange Natali; Tolosa, Nori Graciela
- Año de publicación
- 2015
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Intestinal Ca2+ absorption is a crucial physiological process for maintaining bone mineralization and Ca2+ homeostasis. It occurs through the transcellular and paracellular pathways. The first route comprises 3 steps: the entrance of Ca2+ across the brush border membranes (BBM) of enterocytes through epithelial Ca2+ channels TRPV6, TRPV5, and Cav1.3; Ca2+ movement from the BBM to the basolateral membranes by binding proteins with high Ca2+ affinity (such as CB9k); and Ca2+ extrusion into the blood. Plasma membrane Ca2+ ATPase (PMCA1b) and sodium calcium exchanger (NCX1) are mainly involved in the exit of Ca2+ from enterocytes. A novel molecule, the 4.1R protein, seems to be a partner of PMCA1b, since both molecules colocalize and interact. The paracellular pathway consists of Ca2+ transport through transmembrane proteins of tight junction structures, such as claudins 2, 12, and 15. There is evidence of crosstalk between the transcellular and paracellular pathways in intestinal Ca2+ transport. When intestinal oxidative stress is triggered, there is a decrease in the expression of several molecules of both pathways that inhibit intestinal Ca2+ absorption. Normalization of redox status in the intestine with drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal Ca2+ transport to control values. Calcitriol [1,25(OH)2D3] is the major controlling hormone of intestinal Ca2+ transport. It increases the gene and protein expression of most of the molecules involved in both pathways. PTH, thyroid hormones, estrogens, prolactin, growth hormone, and glucocorticoids apparently also regulate Ca2+ transport by direct action, indirect mechanism mediated by the increase of renal 1,25(OH)2D3 production, or both. Different physiological conditions, such as growth, pregnancy, lactation, and aging, adjust intestinal Ca2+ absorption according to Ca2+ demands. Better knowledge of the molecular details of intestinal Ca2+ absorption could lead to the development of nutritional and medical strategies for optimizing the efficiency of intestinal Ca2+ absorption and preventing osteoporosis and other pathologies related to Ca2+ metabolism.
Fil: Díaz de Barboza, Gabriela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina
Fil: Guizzardi, Solange Natali. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Tolosa, Nori Graciela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina - Materia
-
INTESTINAL CALCIUM ABSORPTION
TRANSCELLULAR PATHWAY
1,25(OH)2D3
PTH - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/11398
Ver los metadatos del registro completo
id |
CONICETDig_34ca1d671a32b4317cbfc1d619d63fd7 |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/11398 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
network_name_str |
CONICET Digital (CONICET) |
spelling |
Molecular aspects of intestinal calcium absorptionDíaz de Barboza, GabrielaGuizzardi, Solange NataliTolosa, Nori GracielaINTESTINAL CALCIUM ABSORPTIONTRANSCELLULAR PATHWAY1,25(OH)2D3PTHhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Intestinal Ca2+ absorption is a crucial physiological process for maintaining bone mineralization and Ca2+ homeostasis. It occurs through the transcellular and paracellular pathways. The first route comprises 3 steps: the entrance of Ca2+ across the brush border membranes (BBM) of enterocytes through epithelial Ca2+ channels TRPV6, TRPV5, and Cav1.3; Ca2+ movement from the BBM to the basolateral membranes by binding proteins with high Ca2+ affinity (such as CB9k); and Ca2+ extrusion into the blood. Plasma membrane Ca2+ ATPase (PMCA1b) and sodium calcium exchanger (NCX1) are mainly involved in the exit of Ca2+ from enterocytes. A novel molecule, the 4.1R protein, seems to be a partner of PMCA1b, since both molecules colocalize and interact. The paracellular pathway consists of Ca2+ transport through transmembrane proteins of tight junction structures, such as claudins 2, 12, and 15. There is evidence of crosstalk between the transcellular and paracellular pathways in intestinal Ca2+ transport. When intestinal oxidative stress is triggered, there is a decrease in the expression of several molecules of both pathways that inhibit intestinal Ca2+ absorption. Normalization of redox status in the intestine with drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal Ca2+ transport to control values. Calcitriol [1,25(OH)2D3] is the major controlling hormone of intestinal Ca2+ transport. It increases the gene and protein expression of most of the molecules involved in both pathways. PTH, thyroid hormones, estrogens, prolactin, growth hormone, and glucocorticoids apparently also regulate Ca2+ transport by direct action, indirect mechanism mediated by the increase of renal 1,25(OH)2D3 production, or both. Different physiological conditions, such as growth, pregnancy, lactation, and aging, adjust intestinal Ca2+ absorption according to Ca2+ demands. Better knowledge of the molecular details of intestinal Ca2+ absorption could lead to the development of nutritional and medical strategies for optimizing the efficiency of intestinal Ca2+ absorption and preventing osteoporosis and other pathologies related to Ca2+ metabolism.Fil: Díaz de Barboza, Gabriela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; ArgentinaFil: Guizzardi, Solange Natali. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Tolosa, Nori Graciela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaW J G Press2015-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/11398Díaz de Barboza, Gabriela; Guizzardi, Solange Natali; Tolosa, Nori Graciela; Molecular aspects of intestinal calcium absorption; W J G Press; World Journal Of Gastroenterology; 21; 23; 6-2015; 7142-71541007-93272219-2840enginfo:eu-repo/semantics/altIdentifier/url/http://www.wjgnet.com/1007-9327/full/v21/i23/7142.htminfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476875/info:eu-repo/semantics/altIdentifier/url/http://dx.doi.org/10.3748/WJG.v21.i23.7142info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:54:30Zoai:ri.conicet.gov.ar:11336/11398instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:54:30.809CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Molecular aspects of intestinal calcium absorption |
title |
Molecular aspects of intestinal calcium absorption |
spellingShingle |
Molecular aspects of intestinal calcium absorption Díaz de Barboza, Gabriela INTESTINAL CALCIUM ABSORPTION TRANSCELLULAR PATHWAY 1,25(OH)2D3 PTH |
title_short |
Molecular aspects of intestinal calcium absorption |
title_full |
Molecular aspects of intestinal calcium absorption |
title_fullStr |
Molecular aspects of intestinal calcium absorption |
title_full_unstemmed |
Molecular aspects of intestinal calcium absorption |
title_sort |
Molecular aspects of intestinal calcium absorption |
dc.creator.none.fl_str_mv |
Díaz de Barboza, Gabriela Guizzardi, Solange Natali Tolosa, Nori Graciela |
author |
Díaz de Barboza, Gabriela |
author_facet |
Díaz de Barboza, Gabriela Guizzardi, Solange Natali Tolosa, Nori Graciela |
author_role |
author |
author2 |
Guizzardi, Solange Natali Tolosa, Nori Graciela |
author2_role |
author author |
dc.subject.none.fl_str_mv |
INTESTINAL CALCIUM ABSORPTION TRANSCELLULAR PATHWAY 1,25(OH)2D3 PTH |
topic |
INTESTINAL CALCIUM ABSORPTION TRANSCELLULAR PATHWAY 1,25(OH)2D3 PTH |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Intestinal Ca2+ absorption is a crucial physiological process for maintaining bone mineralization and Ca2+ homeostasis. It occurs through the transcellular and paracellular pathways. The first route comprises 3 steps: the entrance of Ca2+ across the brush border membranes (BBM) of enterocytes through epithelial Ca2+ channels TRPV6, TRPV5, and Cav1.3; Ca2+ movement from the BBM to the basolateral membranes by binding proteins with high Ca2+ affinity (such as CB9k); and Ca2+ extrusion into the blood. Plasma membrane Ca2+ ATPase (PMCA1b) and sodium calcium exchanger (NCX1) are mainly involved in the exit of Ca2+ from enterocytes. A novel molecule, the 4.1R protein, seems to be a partner of PMCA1b, since both molecules colocalize and interact. The paracellular pathway consists of Ca2+ transport through transmembrane proteins of tight junction structures, such as claudins 2, 12, and 15. There is evidence of crosstalk between the transcellular and paracellular pathways in intestinal Ca2+ transport. When intestinal oxidative stress is triggered, there is a decrease in the expression of several molecules of both pathways that inhibit intestinal Ca2+ absorption. Normalization of redox status in the intestine with drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal Ca2+ transport to control values. Calcitriol [1,25(OH)2D3] is the major controlling hormone of intestinal Ca2+ transport. It increases the gene and protein expression of most of the molecules involved in both pathways. PTH, thyroid hormones, estrogens, prolactin, growth hormone, and glucocorticoids apparently also regulate Ca2+ transport by direct action, indirect mechanism mediated by the increase of renal 1,25(OH)2D3 production, or both. Different physiological conditions, such as growth, pregnancy, lactation, and aging, adjust intestinal Ca2+ absorption according to Ca2+ demands. Better knowledge of the molecular details of intestinal Ca2+ absorption could lead to the development of nutritional and medical strategies for optimizing the efficiency of intestinal Ca2+ absorption and preventing osteoporosis and other pathologies related to Ca2+ metabolism. Fil: Díaz de Barboza, Gabriela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina Fil: Guizzardi, Solange Natali. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Tolosa, Nori Graciela. Universidad Nacional de Cordoba. Facultad de Medicina. Catedra de Bioquimica y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina |
description |
Intestinal Ca2+ absorption is a crucial physiological process for maintaining bone mineralization and Ca2+ homeostasis. It occurs through the transcellular and paracellular pathways. The first route comprises 3 steps: the entrance of Ca2+ across the brush border membranes (BBM) of enterocytes through epithelial Ca2+ channels TRPV6, TRPV5, and Cav1.3; Ca2+ movement from the BBM to the basolateral membranes by binding proteins with high Ca2+ affinity (such as CB9k); and Ca2+ extrusion into the blood. Plasma membrane Ca2+ ATPase (PMCA1b) and sodium calcium exchanger (NCX1) are mainly involved in the exit of Ca2+ from enterocytes. A novel molecule, the 4.1R protein, seems to be a partner of PMCA1b, since both molecules colocalize and interact. The paracellular pathway consists of Ca2+ transport through transmembrane proteins of tight junction structures, such as claudins 2, 12, and 15. There is evidence of crosstalk between the transcellular and paracellular pathways in intestinal Ca2+ transport. When intestinal oxidative stress is triggered, there is a decrease in the expression of several molecules of both pathways that inhibit intestinal Ca2+ absorption. Normalization of redox status in the intestine with drugs such as quercetin, ursodeoxycholic acid, or melatonin return intestinal Ca2+ transport to control values. Calcitriol [1,25(OH)2D3] is the major controlling hormone of intestinal Ca2+ transport. It increases the gene and protein expression of most of the molecules involved in both pathways. PTH, thyroid hormones, estrogens, prolactin, growth hormone, and glucocorticoids apparently also regulate Ca2+ transport by direct action, indirect mechanism mediated by the increase of renal 1,25(OH)2D3 production, or both. Different physiological conditions, such as growth, pregnancy, lactation, and aging, adjust intestinal Ca2+ absorption according to Ca2+ demands. Better knowledge of the molecular details of intestinal Ca2+ absorption could lead to the development of nutritional and medical strategies for optimizing the efficiency of intestinal Ca2+ absorption and preventing osteoporosis and other pathologies related to Ca2+ metabolism. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-06 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/11398 Díaz de Barboza, Gabriela; Guizzardi, Solange Natali; Tolosa, Nori Graciela; Molecular aspects of intestinal calcium absorption; W J G Press; World Journal Of Gastroenterology; 21; 23; 6-2015; 7142-7154 1007-9327 2219-2840 |
url |
http://hdl.handle.net/11336/11398 |
identifier_str_mv |
Díaz de Barboza, Gabriela; Guizzardi, Solange Natali; Tolosa, Nori Graciela; Molecular aspects of intestinal calcium absorption; W J G Press; World Journal Of Gastroenterology; 21; 23; 6-2015; 7142-7154 1007-9327 2219-2840 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://www.wjgnet.com/1007-9327/full/v21/i23/7142.htm info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476875/ info:eu-repo/semantics/altIdentifier/url/http://dx.doi.org/10.3748/WJG.v21.i23.7142 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
W J G Press |
publisher.none.fl_str_mv |
W J G Press |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
_version_ |
1842269289371926528 |
score |
13.13397 |