Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes

A selective primary culture of fetal rat hepatocytes was established in our laboratory in order to elucidate the molecular mechanisms of action of different factors and conditions on insulin-like growth factor (IGF)-I and -II gene expression during the perinatal period of the rat. In this model we report that, in a serum-free condition and the presence of non-stimulatory doses of insulin, 5–20 mM glucose evoked an increase of IGF-I and -II mRNA abundance. Glucose regulated in a parallel manner IGF peptide secretion, and an excellent correlation was observed between IGF-I and -II mRNA and IGF-I and -II peptide levels in the conditioned media in response to the carbohydrate. The experiment with 2-deoxyglucose suggests that glucose 6-phosphate, but not its further metabolism, is necessary for the induction of IGF transcript abundance in cultured fetal hepatocytes. Finally, the glucose-induced rise in IGF-II mRNA, the main IGF in fetal stages, was mediated by stimulation of gene transcription and increased transcript stability. The results support the idea that IGFs belong to a family of genes that are positively regulated by glucose.

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Main Authors: Goya, Luis, Puente, Ana de la, Ramos, Sonia, Martín, M. Ángeles, Escrivá, Fernando, Pascual-Leone, A. M.
Other Authors: Comunidad de Madrid
Format: artículo biblioteca
Language:English
Published: American Society for Biochemistry and Molecular Biology 1999
Online Access:http://hdl.handle.net/10261/190134
http://dx.doi.org/10.13039/100012818
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spelling dig-ictan-es-10261-1901342022-01-26T09:13:46Z Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes Goya, Luis Puente, Ana de la Ramos, Sonia Martín, M. Ángeles Escrivá, Fernando Pascual-Leone, A. M. Comunidad de Madrid Ministerio de Educación y Ciencia (España) A selective primary culture of fetal rat hepatocytes was established in our laboratory in order to elucidate the molecular mechanisms of action of different factors and conditions on insulin-like growth factor (IGF)-I and -II gene expression during the perinatal period of the rat. In this model we report that, in a serum-free condition and the presence of non-stimulatory doses of insulin, 5–20 mM glucose evoked an increase of IGF-I and -II mRNA abundance. Glucose regulated in a parallel manner IGF peptide secretion, and an excellent correlation was observed between IGF-I and -II mRNA and IGF-I and -II peptide levels in the conditioned media in response to the carbohydrate. The experiment with 2-deoxyglucose suggests that glucose 6-phosphate, but not its further metabolism, is necessary for the induction of IGF transcript abundance in cultured fetal hepatocytes. Finally, the glucose-induced rise in IGF-II mRNA, the main IGF in fetal stages, was mediated by stimulation of gene transcription and increased transcript stability. The results support the idea that IGFs belong to a family of genes that are positively regulated by glucose. This work was supported by Direccion General de Investigacion, Ciencia y Tecnologia, Ministerio de Educacion y Ciencia, Spain, Grants PB94-0030 and PM 97-0017 and by Comunidad Autonoma de Madrid Grant 08.5/0009/1997. Peer reviewed 2019-09-06T11:56:46Z 2019-09-06T11:56:46Z 1999 artículo http://purl.org/coar/resource_type/c_6501 Journal of Biological Chemistry 274(35): 24633-24640 (1999) 0021-9258 http://hdl.handle.net/10261/190134 10.1074/jbc.274.35.24633 1083-351X http://dx.doi.org/10.13039/100012818 en Publisher's version https://doi.org/10.1074/jbc.274.35.24633 Sí open American Society for Biochemistry and Molecular Biology
institution ICTAN ES
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description A selective primary culture of fetal rat hepatocytes was established in our laboratory in order to elucidate the molecular mechanisms of action of different factors and conditions on insulin-like growth factor (IGF)-I and -II gene expression during the perinatal period of the rat. In this model we report that, in a serum-free condition and the presence of non-stimulatory doses of insulin, 5–20 mM glucose evoked an increase of IGF-I and -II mRNA abundance. Glucose regulated in a parallel manner IGF peptide secretion, and an excellent correlation was observed between IGF-I and -II mRNA and IGF-I and -II peptide levels in the conditioned media in response to the carbohydrate. The experiment with 2-deoxyglucose suggests that glucose 6-phosphate, but not its further metabolism, is necessary for the induction of IGF transcript abundance in cultured fetal hepatocytes. Finally, the glucose-induced rise in IGF-II mRNA, the main IGF in fetal stages, was mediated by stimulation of gene transcription and increased transcript stability. The results support the idea that IGFs belong to a family of genes that are positively regulated by glucose.
author2 Comunidad de Madrid
author_facet Comunidad de Madrid
Goya, Luis
Puente, Ana de la
Ramos, Sonia
Martín, M. Ángeles
Escrivá, Fernando
Pascual-Leone, A. M.
format artículo
author Goya, Luis
Puente, Ana de la
Ramos, Sonia
Martín, M. Ángeles
Escrivá, Fernando
Pascual-Leone, A. M.
spellingShingle Goya, Luis
Puente, Ana de la
Ramos, Sonia
Martín, M. Ángeles
Escrivá, Fernando
Pascual-Leone, A. M.
Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
author_sort Goya, Luis
title Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
title_short Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
title_full Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
title_fullStr Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
title_full_unstemmed Regulation of insulin-like growth factor-I and -II by glucose in primary cultures of fetal rat hepatocytes
title_sort regulation of insulin-like growth factor-i and -ii by glucose in primary cultures of fetal rat hepatocytes
publisher American Society for Biochemistry and Molecular Biology
publishDate 1999
url http://hdl.handle.net/10261/190134
http://dx.doi.org/10.13039/100012818
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