Phosphoenolpyruvate Carboxykinase (GTP): the Gene and the Enzyme

Hanson, Richard W.; Patel, Yashomati M.

doi:10.1002/9780470123157.ch6

Cited by 82 publications

(82 citation statements)

References 189 publications

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“…The activity of PEPCK is only controlled at the level of transcription as there are no known allosteric modifiers. 43 In mammals, the gene encoding the cytosolic isoform is under nutritional and hormonal control, which is not the case of the mitochondrial isoform, known to be constitutively expressed. This feature may probably be extended to zebrafish inasmuch as cytosolic PEPCK gene expression exhibited to a 30-fold decrease between 6 and 24 h after the meal, whereas mPEPCK is poorly downregulated during the same period (1.2-fold increase).…”

Section: Seiliez Et Almentioning

confidence: 99%

Postprandial Regulation of Growth- and Metabolism-Related Factors in Zebrafish

et al. 2013

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Zebrafish (Danio rerio) have been proposed as a possible model organism for nutritional physiology. However, this potential has not yet been realized and studies on the field remain scarce. In this work, we investigated in this species the effect of a single meal as well as that of an increase in the ratio of dietary carbohydrates/proteins on the postprandial expression of several hepatic and muscle metabolism-related genes and proteins. Fish were fed once either a commercial diet (experiment 1) or one of two experimental diets (experiment 2) containing different protein and carbohydrate levels after 72 h of starvation. Refeeding induced the postprandial expression of genes of glycolysis (GK, HK1) and lipogenesis (FAS, G6PDH, ACCa) and inhibited those of gluconeogenesis (cPEPCK) and beta-oxidation (CPT1b) in the viscera. In the muscle, refeeding increased transcript levels of myogenesis (Myf5, Myogenin), inhibited those of Ub-proteasomal proteolytic system (Atrogin1, Murf1a, Murf1b), and induced the activation of key signaling factors of protein synthesis (Akt, 4EBP1, S6K1, S6). However, diet composition had a low impact on the studied factors. Together, these results highlight some specificity of the zebrafish metabolism and demonstrate the interest and the limits of this species as a model organism for nutritional physiology studies.

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Section: Seiliez Et Almentioning

confidence: 99%

Postprandial Regulation of Growth- and Metabolism-Related Factors in Zebrafish

et al. 2013

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“…PEPCK gene expression is increased not only in diabetes but also in hyperthyroidism and in various nutritional states such as high protein diets and fasting (Hanson and Reshef 1997). The G6Pase gene is mutated in glycogen storage disease type 1a and type1b (van Schaftingen and Gerin 2002).…”

Section: Introductionmentioning

confidence: 99%

Hormonal regulation of gluconeogenic gene transcription in the liver

2010

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Glucose homeostasis in mammals is achieved by the actions of counterregulatory hormones, namely insulin, glucagon and glucocorticoids. Glucose levels in the circulation are regulated by the liver, the metabolic centre which produces glucose when it is scarce in the blood. This process is catalysed by two rate-limiting enzymes, phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) whose gene expression is regulated by hormones. Hormone response units (HRUs) present in the two genes integrate signals from various signalling pathways triggered by hormones. How such domains are arranged in the regulatory region of these two genes, how this complex regulation is accomplished and the latest advancements in the field are discussed in this review.

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“…Rate-limited enzymes of gluconeogenesis, such as glucose-6-phosphate (G6Pase), fructose-1, 6-bisphosphatase (FBPase), and phosphoenolpyruvate carboxykinase (PEPCK) [26][27][28], also play important roles in glucose metabolism. Expression of these mRNAs was increased in diabetic, but not in pre-diabetic SDT rats [4]; hence the key enzymes of gluconeogenesis are upregulated in SDT rats after progression of diabetes.…”

Section: Glucose Metabolismmentioning

confidence: 99%

Glucose and Lipid Metabolism in Spontaneously Diabetic Torii Rat

Mera¹

2011

TODIAJ

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Abstract:The impairment of glucose metabolism may lead to type 2 diabetes and the malfunction of lipid metabolism contributing to metabolic syndrome, which increases risk of heart disease, vascular disease, and type 2 diabetes. Our previous study provided evidence for involvement of hepatic glucose metabolic disorder in onset and progress of diabetes in Spontaneously Diabetic Torii (SDT) rats. As it is increasingly important to elucidate the mechanism of onset of diabetes and to develop drugs to prevent diabetic pathological progress, SDT rat should offer a highly useful model of spontaneous diabetic onset for such studies. In addition, abnormality in triglyceride (TG) absorption and impaired lipid catabolism antecedent to hypoinsulinemia/hyperglycemia seem to cause postprandial hypertriglyceridemia in SDT rat; hence, the characteristics of lipid metabolism in SDT rat can be useful in studies of diabetic hypertriglyceridemia and TG metabolism.

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Phosphoenolpyruvate Carboxykinase (GTP): the Gene and the Enzyme

Cited by 82 publications

References 189 publications

Postprandial Regulation of Growth- and Metabolism-Related Factors in Zebrafish

Postprandial Regulation of Growth- and Metabolism-Related Factors in Zebrafish

Hormonal regulation of gluconeogenic gene transcription in the liver

Glucose and Lipid Metabolism in Spontaneously Diabetic Torii Rat

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