In vivo regulation of glycolytic and gluconeogenic enzyme gene expression in newborn rat liver.

Lyonnet, Stanislas; Coupé, Christine; Girard, Jean; Kahn, Axel; Münnich, Arnold

doi:10.1172/jci113506

Cited by 40 publications

(27 citation statements)

References 51 publications

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“…2B); the increase was about 1.5-fold between days 18.5 and 21.5 and was 1.7-fold between day 21.5 and day 1 after birth ( n = 2). The P-pyruvate CK gene, used as positive control, also showed an acute increase during the same period of time, as expected [30]. These results demonstrate that the elevation in ASS mRNA level and in corresponding enzyme activity measured during the perinatal period was primarily caused by an increased transcriptional activity of the ASS gene.…”

Section: -Actinsupporting

confidence: 84%

Regulation of Argininosuccinate Synthetase mRNA Level in Rat Foetal Hepatocytes

Bourgeois

Harlin

Renouf

et al. 1997

European Journal of Biochemistry

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Expression of the hepatic gene for argininosuccinate synthase (ASS), one of the key enzymes of the urea cycle, was analysed during the perinatal period in the rat. To this end, the amount of specific mRNA was measured in the liver at various stages of development and in cultured foetal hepatocytes maintained in different hormonal conditions. The ASS mRNA was first detected in 15.5-day foetuses and its level increased concomitantly with a rise in the enzyme activity, suggesting that the appearance of the ASS activity reflects the turning on of specific gene transcription. This was demonstrated by run-on assay which showed an enhanced rate of transcription of the ASS gene during the perinatal period. When foetal hepatocytes were cultured with dexamethasone, a dose-dependent increase in ASS mRNA was measured, which was completely abolished by actinomycin D addition. The transcription rate of the gene was increased about twofold in the presence of the steroid, as measured by nuclear run-on assay. This transcriptional action could additionally require a protein factor since it could be inhibited by the simultaneous addition of puromycin. Insulin or glucagon respectively repressed or enhanced the dexamethasone-induced accumulation of ASS mRNA when added simultaneously with the steroid for 24 h. This developmental regulation of the ASS mRNA by glucocorticoids, insulin and glucagon could account for the modulation of the enzyme activity previously observed in vivo and in vitro in the foetal liver.Keywords: argininosuccinate synthetase; mRNA ; gene transcription ; cultured foetal hepatocyte; glucocorticoid.Argininosuccinate synthetase (ASS) catalyses the synthesis of argininosuccinate from aspartate and citrulline, and is one of the key enzymes of the urea cycle in Mammals [l]. This enzyme is expressed in many tissues, with highest expression in the liver and in the kidney, where it plays a role in the arginine synthesis [2], and in the testis [3].Regulation of expression of ASS in the adult rat liver appears complex since increased protein content in the diet, prolonged starvation [4] and administration of glucocorticoids or glucagon have been shown to increase its activity both in vivo [5, 61 and in vitro [7, 81. Most of these treatments also produced an accumulation of specific mRNA [9-111. The expression of this gene was shown to be also regulated by amino acids since it was stimulated by glutamine addition in cultured rat hepatocytes [12] and repressed by arginine in cultured human cellsIn the late foetal period, the urea cycle enzymes are actively synthesized in the liver and this differentiation largely depends on the foetal endocrine state [14-161. Previous studies have shown that the ASS activity appeared in the foetal rat liver during the last days of gestation and that its development depended on the presence of foetal adrenals [14, 151 and on plasma levels of glucagon and insulin [17]. In particular ASS activity did not ~3 1 . The aim of the present work was to characterize the expression of the gene of ASS ...

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Section: -Actinsupporting

confidence: 84%

Regulation of Argininosuccinate Synthetase mRNA Level in Rat Foetal Hepatocytes

Bourgeois

Harlin

Renouf

et al. 1997

European Journal of Biochemistry

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“…This was mainly revealed at crucial stages of development characterized by dramatic changes in diet and hormone levels. Glucagon might increase the expression of the apo-E gene by protein-kinase-Amediated process as already described for the phosphoenolpyruvate-carboxykinase gene [30] and insulin might counteract the inducing effect of glucagon. In order to confirm such an hypothesis and to discriminate among the numerous nutritional and hormonal factors regulating apo-E gene expression, and to determine whether the hepatocyte is the direct target of such factors, further studies are in progress with cultured rat hepatocytes.…”

Section: Effect Of Fasting and Glucose Feeding On Plasmu Hormone Levelsmentioning

confidence: 73%

“…Strikingly, in 5-day-old glucose-fed rats, plasma glucagon level was within the same range as that in the fasted group (220 _+ 18 pg/ml and 21 3 k 36 pg/ml respectively). But, as plasma insulin level reached 92 pU/ml, the insulin/glucagon molar ratio rose to 9.5/1 in fasted rats [30].…”

Section: Effect Of Fasting and Glucose Feeding On Plasmu Hormone Levelsmentioning

confidence: 87%

Apolipoprotein‐E‐gene expression in rat liver during development in relation to insulin and glucagon

Mangeney¹,

Cardot²,

Lyonnet³

et al. 1989

European Journal of Biochemistry

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An apolipoprotein-E (apo-E) cDNA probe, cloned by immunoscreening of a l G T l l rat liver cDNA library, was used to further characterize the expression of the apo-E gene in rat liver during development, in relation to plasma insulin and glucagon levels. The apo-E mRNA level was low in fetus liver, then abruptly increased at birth and rose further during the suckling period. It returned to the level at birth in 10-week-old adults. These variations were paralleled with dramatic changes in plasma glucagon, which rose at birth and remained high during suckling. At the same time, the insulin/glucagon molar ratio fell.Administration of N6,02-dibutyryl CAMP to 5-day-old rats resulted in a significant induction of liver apo-E mRNA. Moreover, liver apo-E mRNA rose in 10-h-fasted suckling rats as compared to controls, while plasma glucagon increased and the insulin/glucagon ratio decreased. Conversely, glucose feeding of suckling rats did not induce any increase in liver apo-E mRNA, the insulin/glucagon ratio was 10-fold higher than in fasted animals.Our results are consistent with liver apo-E gene expression being under the control of plasma glucagon and of the glucagon/insulin balance. Apo E is a major protein component of lipoproteins [l]. It is responsible for mediating the interaction of specific lipoproteins with extrahepatic and hepatic apo-B/E receptors and the hepatic apo-E receptors [l, 21.The complete sequence of apo-E cDNA, and the structure of its gene, have been reported for rats and humans [3 -61. Apo-E gene expression has been found at a substantial level in brain, adrenals and other peripheral tissues in rats, rabbits, primates and humans [7 -111. Nevertheless, apo E is mainly synthesized in the liver and represents about 1 YO of the total liver mRNA [12]. However, little information is available on the regulation of apo-E-gene expression.

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“…2, hepatic PK mRNA levels were markedly decreased on day 1 in the SF rats, indicating a deceleration of glycolysis in the liver at the beginning of the spaced feeding phase. The deceleration of glycolysis was considered to be due to the marked decrease in plasma glucose levels caused by the severe starvation (Lyonnet et al, 1988). On the other hand, on day 35, PK mRNA levels were comparable to those in the ALF rats, indicating that the deceleration of glycolysis was resolved by metabolic adaptation to the spaced feeding condition.…”

Section: Discussionmentioning

confidence: 96%

Effects of spaced feeding on gene expression of hepatic transaminase and gluconeogenic enzymes in rats

et al. 2011

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-Blood alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities are widely used as sensitive markers of liver toxicity. However, these activities are also recognized to be altered by hormonal and nutritional modifications. We investigated the relationships between the activity and gene expression of the hepatic transaminases and the state of hepatic amino acid/glucose/fatty acid metabolism in the ad libitum fed (ALF) and spaced-fed (SF) rats. Acceleration of hepatic gluconeogenesis and fatty acid oxidation was noted in the SF rats. Expression of hepatic clock gene was also altered in the SF rats. Hepatic transaminase activities in the SF rats were higher than those in the ALF rats. These alterations were due to increases in the synthesis of hepatic ALT and AST proteins. In conclusion, the increased transaminase protein synthesis in the liver of the SF rats was considered to be related to the acceleration of hepatic gluconeogenesis under the conditions of spaced feeding.

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In vivo regulation of glycolytic and gluconeogenic enzyme gene expression in newborn rat liver.

Cited by 40 publications

References 51 publications

Regulation of Argininosuccinate Synthetase mRNA Level in Rat Foetal Hepatocytes

Regulation of Argininosuccinate Synthetase mRNA Level in Rat Foetal Hepatocytes

Apolipoprotein‐E‐gene expression in rat liver during development in relation to insulin and glucagon

Effects of spaced feeding on gene expression of hepatic transaminase and gluconeogenic enzymes in rats

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