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Titolo:
Mice with a deletion in the gene for CCAAT/enhancer-binding protein beta have an attenuated response to cAMP and impaired carbohydrate metabolism
Autore:
Croniger, CM; Millward, C; Yang, JQ; Kawai, Y; Arinze, IJ; Liu, S; Harada-Shiba, M; Chakravarty, K; Friedman, JE; Poli, V; Hanson, RW;
Indirizzi:
Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Case Western Reserve Univ, Sch Med, Dept Nutr, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Meharry Med Coll, Dept Biochem, Nashville, TN 37208 USA Meharry Med Coll Nashville TN USA 37208 Biochem, Nashville, TN 37208 USA Univ Dundee, Dept Mol Biol, Dundee DD1 4HN, Scotland Univ Dundee Dundee Scotland DD1 4HN t Mol Biol, Dundee DD1 4HN, Scotland
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 1, volume: 276, anno: 2001,
pagine: 629 - 638
SICI:
0021-9258(20010105)276:1<629:MWADIT>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
PHOSPHOENOLPYRUVATE CARBOXYKINASE GTP; ALPHA KNOCKOUT MICE; KINASE SUBUNITS; RAT; TRANSCRIPTION; EXPRESSION; PHOSPHODIESTERASE; PROMOTER; LIVER; IDENTIFICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Croniger, CM Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 H 44106 USA
Citazione:
C.M. Croniger et al., "Mice with a deletion in the gene for CCAAT/enhancer-binding protein beta have an attenuated response to cAMP and impaired carbohydrate metabolism", J BIOL CHEM, 276(1), 2001, pp. 629-638

Abstract

Fifty percent of the mice homozygous for a deletion in the gene for CCAAT/enhancer-binding protein beta (C/ EBP beta-/- mice; B phenotype) die within1 to 2 h after birth of hypoglycemia. They do not mobilize their hepatic glycogen or induce the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK). Administration of cAMP resulted in mobilization of glycogen, induction of PEPCK mRNA, and a normal blood glucose; these mice survived beyond 2h postpartum. Adult C/EBP beta-/- mice (A phenotype) also had difficulty in maintaining blood glucose levels during starvation. Fasting these mice for 16 or 30 h resulted in lower levels of hepatic PEPCK mRNA, blood glucose,beta -hydroxybutyrate, blood urea nitrogen, and gluconeogenesis when compared with control mice. The concentration of hepatic cAMP in these mice was 50% of controls, but injection of theophylline, together with glucagon, resulted in a normal cAMP levels. Agonists (glucagon, epinephrine, and isoproterenol) and other effecters of activation of adenylyl cyclase were the samein liver membranes isolated from C/EBP beta-/- mice and littermates, The hepatic activity of cAMP-dependent protein kinase was 80% of wild type mice. There was a 79% increase in the concentration of RI alpha and 27% increasein RII alpha in the particulate fraction of the livers of C/EBP beta-/- mice relative to wild type mice, with no change in the catalytic subunit (C alpha). Thus, a 45% increase in hepatic cAMP (relative to the wild type) would be required in C/EBP beta-/- mice to activate protein kinase A by 50%. In addition, the total activity of phosphodiesterase in the livers of C/EBP beta-/- mice, as well as the concentration of mRNA for phosphodiesterase 3A(PDE3A) and PDE3B was approximately 25% higher than in control animals, suggesting accelerated degradation of cAMP. C/EBP beta influences the regulation of carbohydrate metabolism by altering the level of hepatic cAMP and the activity of protein kinase A.

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Documento generato il 09/07/20 alle ore 18:11:02