The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats
- Autores
- Montes, Monica Raquel; Chicco, Adriana Graciela; Bolzon, Yolanda Ana Rosa
- Año de publicación
- 2000
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Male Wistar rats chronically (15 weeks) fed a sucrose-rich diet (SRD; 63% w/w) developed hypertriglyceridemia and impaired glucose homeostasis. Hearts from these animals were isolated and perfused using the Langendorff recirculating method. Glucose at levels similar to those found in the animal in vivo was used as the only exogenous substrate. The hearts were perfused for 30 minutes in the presence or absence of insulin (30 mU/mL) in the perfusion medium. In the absence of the hormone, glucose uptake was impaired and the glucose utilization was reduced, with a significant increase of lactate release. Glucose oxidation, which was estimated from the activation state of the enzyme pyruvate dehydrogenase complex (PDHc), was depressed mainly due to both an increase of PDH kinase and a decrease of PDHa (active form of PDHc) activities. Although the addition of insulin in the perfusion medium improved the above parameters, it was unable to normalize them. The present results suggest that at least two different mechanisms might contribute to insulin resistance and to the impaired glucose metabolism in the perfused hearts of the dyslipemic SRD-fed animals: (1) reduced basal and insulin-stimulated glucose uptake and its utilization or (2) increased availability and oxidation of lipids (low PDHa and high PDH kinase activities), which in turn decrease glucose uptake and utilization. Thus, this nutritional experimental model may be useful to study how impaired glucose homeostasis, increases plasma free fatty acid levels and hypertriglyceridemia could contribute to heart tissue malfunction. Copyright (C) 2000 Elsevier Science Inc.
Fil: Montes, Monica Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina
Fil: Chicco, Adriana Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina
Fil: Bolzon, Yolanda Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina - Materia
-
Glucose Intolerance
Hypertriglyceridemia
Insulin Resistance
Isolated Rat Heart
Sucrose-Rich Diet - 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:11336/72040
Ver los metadatos del registro completo
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The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic ratsMontes, Monica RaquelChicco, Adriana GracielaBolzon, Yolanda Ana RosaGlucose IntoleranceHypertriglyceridemiaInsulin ResistanceIsolated Rat HeartSucrose-Rich Diethttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Male Wistar rats chronically (15 weeks) fed a sucrose-rich diet (SRD; 63% w/w) developed hypertriglyceridemia and impaired glucose homeostasis. Hearts from these animals were isolated and perfused using the Langendorff recirculating method. Glucose at levels similar to those found in the animal in vivo was used as the only exogenous substrate. The hearts were perfused for 30 minutes in the presence or absence of insulin (30 mU/mL) in the perfusion medium. In the absence of the hormone, glucose uptake was impaired and the glucose utilization was reduced, with a significant increase of lactate release. Glucose oxidation, which was estimated from the activation state of the enzyme pyruvate dehydrogenase complex (PDHc), was depressed mainly due to both an increase of PDH kinase and a decrease of PDHa (active form of PDHc) activities. Although the addition of insulin in the perfusion medium improved the above parameters, it was unable to normalize them. The present results suggest that at least two different mechanisms might contribute to insulin resistance and to the impaired glucose metabolism in the perfused hearts of the dyslipemic SRD-fed animals: (1) reduced basal and insulin-stimulated glucose uptake and its utilization or (2) increased availability and oxidation of lipids (low PDHa and high PDH kinase activities), which in turn decrease glucose uptake and utilization. Thus, this nutritional experimental model may be useful to study how impaired glucose homeostasis, increases plasma free fatty acid levels and hypertriglyceridemia could contribute to heart tissue malfunction. Copyright (C) 2000 Elsevier Science Inc.Fil: Montes, Monica Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; ArgentinaFil: Chicco, Adriana Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; ArgentinaFil: Bolzon, Yolanda Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; ArgentinaElsevier Science Inc2000-01info: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/11336/72040Montes, Monica Raquel; Chicco, Adriana Graciela; Bolzon, Yolanda Ana Rosa; The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats; Elsevier Science Inc; Journal Of Nutritional Biochemistry; 11; 1; 1-2000; 30-370955-2863CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0955286399000686info:eu-repo/semantics/altIdentifier/doi/10.1016/S0955-2863(99)00068-6info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:58:41Zoai:ri.conicet.gov.ar:11336/72040instacron: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 09:58:41.489CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
title |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
spellingShingle |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats Montes, Monica Raquel Glucose Intolerance Hypertriglyceridemia Insulin Resistance Isolated Rat Heart Sucrose-Rich Diet |
title_short |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
title_full |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
title_fullStr |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
title_full_unstemmed |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
title_sort |
The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats |
dc.creator.none.fl_str_mv |
Montes, Monica Raquel Chicco, Adriana Graciela Bolzon, Yolanda Ana Rosa |
author |
Montes, Monica Raquel |
author_facet |
Montes, Monica Raquel Chicco, Adriana Graciela Bolzon, Yolanda Ana Rosa |
author_role |
author |
author2 |
Chicco, Adriana Graciela Bolzon, Yolanda Ana Rosa |
author2_role |
author author |
dc.subject.none.fl_str_mv |
Glucose Intolerance Hypertriglyceridemia Insulin Resistance Isolated Rat Heart Sucrose-Rich Diet |
topic |
Glucose Intolerance Hypertriglyceridemia Insulin Resistance Isolated Rat Heart Sucrose-Rich Diet |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.3 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Male Wistar rats chronically (15 weeks) fed a sucrose-rich diet (SRD; 63% w/w) developed hypertriglyceridemia and impaired glucose homeostasis. Hearts from these animals were isolated and perfused using the Langendorff recirculating method. Glucose at levels similar to those found in the animal in vivo was used as the only exogenous substrate. The hearts were perfused for 30 minutes in the presence or absence of insulin (30 mU/mL) in the perfusion medium. In the absence of the hormone, glucose uptake was impaired and the glucose utilization was reduced, with a significant increase of lactate release. Glucose oxidation, which was estimated from the activation state of the enzyme pyruvate dehydrogenase complex (PDHc), was depressed mainly due to both an increase of PDH kinase and a decrease of PDHa (active form of PDHc) activities. Although the addition of insulin in the perfusion medium improved the above parameters, it was unable to normalize them. The present results suggest that at least two different mechanisms might contribute to insulin resistance and to the impaired glucose metabolism in the perfused hearts of the dyslipemic SRD-fed animals: (1) reduced basal and insulin-stimulated glucose uptake and its utilization or (2) increased availability and oxidation of lipids (low PDHa and high PDH kinase activities), which in turn decrease glucose uptake and utilization. Thus, this nutritional experimental model may be useful to study how impaired glucose homeostasis, increases plasma free fatty acid levels and hypertriglyceridemia could contribute to heart tissue malfunction. Copyright (C) 2000 Elsevier Science Inc. Fil: Montes, Monica Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina Fil: Chicco, Adriana Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina Fil: Bolzon, Yolanda Ana Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; Argentina |
description |
Male Wistar rats chronically (15 weeks) fed a sucrose-rich diet (SRD; 63% w/w) developed hypertriglyceridemia and impaired glucose homeostasis. Hearts from these animals were isolated and perfused using the Langendorff recirculating method. Glucose at levels similar to those found in the animal in vivo was used as the only exogenous substrate. The hearts were perfused for 30 minutes in the presence or absence of insulin (30 mU/mL) in the perfusion medium. In the absence of the hormone, glucose uptake was impaired and the glucose utilization was reduced, with a significant increase of lactate release. Glucose oxidation, which was estimated from the activation state of the enzyme pyruvate dehydrogenase complex (PDHc), was depressed mainly due to both an increase of PDH kinase and a decrease of PDHa (active form of PDHc) activities. Although the addition of insulin in the perfusion medium improved the above parameters, it was unable to normalize them. The present results suggest that at least two different mechanisms might contribute to insulin resistance and to the impaired glucose metabolism in the perfused hearts of the dyslipemic SRD-fed animals: (1) reduced basal and insulin-stimulated glucose uptake and its utilization or (2) increased availability and oxidation of lipids (low PDHa and high PDH kinase activities), which in turn decrease glucose uptake and utilization. Thus, this nutritional experimental model may be useful to study how impaired glucose homeostasis, increases plasma free fatty acid levels and hypertriglyceridemia could contribute to heart tissue malfunction. Copyright (C) 2000 Elsevier Science Inc. |
publishDate |
2000 |
dc.date.none.fl_str_mv |
2000-01 |
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/11336/72040 Montes, Monica Raquel; Chicco, Adriana Graciela; Bolzon, Yolanda Ana Rosa; The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats; Elsevier Science Inc; Journal Of Nutritional Biochemistry; 11; 1; 1-2000; 30-37 0955-2863 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/72040 |
identifier_str_mv |
Montes, Monica Raquel; Chicco, Adriana Graciela; Bolzon, Yolanda Ana Rosa; The effect of insulin on the uptake and metabolic fate of glucose in isolated perfused hearts of dyslipemic rats; Elsevier Science Inc; Journal Of Nutritional Biochemistry; 11; 1; 1-2000; 30-37 0955-2863 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0955286399000686 info:eu-repo/semantics/altIdentifier/doi/10.1016/S0955-2863(99)00068-6 |
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 |
Elsevier Science Inc |
publisher.none.fl_str_mv |
Elsevier Science Inc |
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 |
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1842269535672991744 |
score |
13.13397 |