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Regulation of malic enzyme gene expression by nutrients, hormones, and growth factors in fetal hepatocyte primary cultures
Author(s) -
Molero Cristina,
Benito Manuel,
Lorenzo Margarita
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041550125
Subject(s) - malic enzyme , insulin , dexamethasone , endocrinology , medicine , biology , enzyme , messenger rna , glucagon , enzyme inducer , gene expression , biochemistry , chemistry , gene , dehydrogenase
Abstract The culture of fetal hepatocytes for 64 h in medium supplemented with 5 mM glucose, T3, insulin, and dexamethasone resulted in the coordinate precocious expression of malic enzyme mRNA, protein, and specific activity. T3 was the main inducer; meanwhile, insulin exerted a small synergistic effect when added with T3. Dexamethasone had a potentiation effect on the T3 response of malic enzyme mRNA expression regardless of the presence of insulin. This effect of dexamethasone on T3 response of malic enzyme mRNA expression was time (64 h) and glucose dependent. Glucagon, and to a greater degree dibutyryl‐cAMP, repressed malic enzyme mRNA as well as protein expression by T3 and dexamethasone, in the absence of insulin. Glucose and other carbon sources such as lactate‐pyruvate or dihydroxyacetone induced the abundance of malic enzyme mRNA in the absence of hormones. Insulin and T3 produced a high accumulation of malic enzyme mRNA in lactate‐pyruvate medium, this effect being decreased by dexamethasone. EGF supressed the induction produced by T3 and dexamethasone on malic enzyme mRNA, while the expression of β‐actin mRNA remained essentially unmodified. © 1993 Wiley‐Liss, Inc.

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