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Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats.

Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Research Abstract Details 

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  • Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Abstract Text:

    t matsudaT Matsuda,t noguchiT Noguchi,m takenakaM Takenaka,k yamadaK Yamada,t tanakaT Tanaka,

    Previous studies have shown that dietary fructose stimulates expression of the L-type pyruvate kinase gene mainly at the post-transcriptional level in diabetic liver, and that this effect may be mediated by a metabolite common to both fructose and glycerol. In the present work, we carried out further studies on the mechanism of fructose induction of L-type isozyme mRNA in the liver, kidney and small intestine of rats. The L-type isozyme mRNA in the kidney of normal and diabetic rats was increased by dietary fructose, the time course of the increase being similar to that observed in the small intestine and liver. The mRNA was not induced in the kidney by dietary glucose or insulin. Glycerol was also a potent inducer of the mRNA in the kidney and liver, but not in the small intestine. These results show that fructose and glycerol induced increase in the mRNA only in organs in which they were metabolized, and thus support the metabolite hypothesis. No other carbohydrates tested increased the level of mRNA in these tissues, except glucose, which increased the level in the small intestine. Thus a molecule that increase the mRNA level may accumulate significantly during metabolism of only certain carbohydrates. Dietary fructose or glycerol slightly stimulated transcription of the gene for the L-type isozyme in diabetic liver, and also in normal and diabetic kidney, but the magnitudes of increase were much lower than those of the mRNA, confirming our previous findings described above. On the other hand, dietary fructose caused marked stimulation of gene transcription in normal rat liver, although the magnitude of its induction of the mRNA was similar to that in diabetic liver. Insulin treatment of fructose-fed diabetic rats also caused a marked increase in the gene transcription without any concomitant change in the mRNA level. Thus, the mechanism of fructose induction of the L-type pyruvate kinase in diabetic liver, which is similar to that found in the kidney, is different from that in normal liver, and this difference is attributable to the difference in the level of insulin.

    Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Publishing Authors By Initials

    t matsudaT Matsuda,t noguchiT Noguchi,m takenakaM Takenaka,k yamadaK Yamada,t tanakaT Tanaka,

    For similar genetic processes: gene expression: transcription, genetic research abstracts see: genetic processes: gene expression: transcription, genetic research

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    Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of biochemistry

    VOLUME: 107

    Page Numbers: 655-60

    Journal Abbreviation: J. Biochem.

    ISSN: 0021-924X

    DAY: 19

    MONTH: Apr

    YEAR: 1990

    Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 376600

    Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Keywords Mesh Terms:

    KEYWORDS: Transcription, Genetic

    MESH TERMS: isolation & purification

    Chemical & Substance for Abstract: Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats. Information

    Substance Name: Pyruvate Kinase

    Registry Number: EC 2.7.1.40

    Grant and Affiliation Information for Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats.

    AFFILIATION: Department of Nutrition and Physiological Chemistry, Osaka University Medical School.

    Country: JAPAN

    JAPAN Research PublicationJAPAN Research Publication

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    MEDLINETA: J Biochem

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