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Disease relevance of Gluconeogenesis


Psychiatry related information on Gluconeogenesis


High impact information on Gluconeogenesis

  • PEPCK-C is absent in fetal liver but appears at birth, concomitant with the capacity for gluconeogenesis [8].
  • Of the 80% of oxygen consumption coupled to ATP synthesis, approximately 25-30% is used by protein synthesis, 19-28% by the Na(+)-K(+)-ATPase, 4-8% by the Ca2(+)-ATPase, 2-8% by the actinomyosin ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA synthesis and substrate cycling also making significant contributions [9].
  • We show here that, while hepatocytes lacking PGC-1alpha are defective in the program of hormone-stimulated gluconeogenesis, the mice have constitutively activated gluconeogenic gene expression that is completely insensitive to normal feeding controls [10].
  • Hda1 also deacetylates subtelomeric domains containing normally repressed genes that are used instead for gluconeogenesis, growth on carbon sources other than glucose, and adverse growth conditions [11].
  • The rate of conversion of lactate to glucose (gluconeogenesis) decreased by 37 percent (P < 0.001), whereas lactate oxidation increased by 25 percent (P < 0.001) [12].

Chemical compound and disease context of Gluconeogenesis


Biological context of Gluconeogenesis


Anatomical context of Gluconeogenesis


Associations of Gluconeogenesis with chemical compounds


Gene context of Gluconeogenesis


Analytical, diagnostic and therapeutic context of Gluconeogenesis


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