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Titolo:
5-Aminoimidazole-4-carboxamide riboside mimics the effects of insulin on the expression of the 2 key gluconeogenic genes PEPCK and glucose-6-phosphatase
Autore:
Lochhead, PA; Salt, IP; Walker, KS; Hardie, DG; Sutherland, C;
Indirizzi:
Univ Dundee, Dept Biochem, Dundee DD1 5EH, Scotland Univ Dundee Dundee Scotland DD1 5EH pt Biochem, Dundee DD1 5EH, Scotland Univ Glasgow, Div Biochem & Mol Biol, Glasgow, Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland Mol Biol, Glasgow, Lanark, Scotland
Titolo Testata:
DIABETES
fascicolo: 6, volume: 49, anno: 2000,
pagine: 896 - 903
SICI:
0012-1797(200006)49:6<896:5RMTEO>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE; FATTY-ACID OXIDATION; RAT-LIVER GLUCOSE-6-PHOSPHATASE; TYROSINE AMINOTRANSFERASE GENE; CELL-PERMEABLE ACTIVATOR; FACTOR-BINDING PROTEIN-1; ACETYL-COA CARBOXYLASE; HEPATOMA-CELLS; IN-VITRO;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Sutherland, C Univ Dundee, Dept Biochem, WTB-MSI Complex, Dundee DD1 5EH, Scotland Univ Dundee WTB-MSI Complex Dundee Scotland DD1 5EH cotland
Citazione:
P.A. Lochhead et al., "5-Aminoimidazole-4-carboxamide riboside mimics the effects of insulin on the expression of the 2 key gluconeogenic genes PEPCK and glucose-6-phosphatase", DIABETES, 49(6), 2000, pp. 896-903

Abstract

Insulin regulates the rate of expression of many hepatic genes, including PEPCK, glucose-6-phosphatase (G6Pase), and glucose-6-phosphate dehydrogenase (G6PDHase). The expression of these genes is also abnormally regulated intype 2 diabetes. We demonstrate here that treatment of hepatoma cells with5-aminoimidazole-4-carboxamide riboside (AICAR), an agent that activates AMP-activated protein kinase (AMPK), mimics the ability of insulin to repress PEPCK gene transcription. It also partially represses G6Pase gene transcription and yet has no effect on the expression of G6PDHase or the constitutively expressed genes cyclophilin or beta-actin. Several lines of evidence suggest that the insulin-mimetic effects of AICAR are mediated by activation of AMPK. Also, insulin does not activate AMPK in H4IIE cells, suggesting that: this protein kinase does not link the insulin receptor to the PEPCK and G6Pase gene promoters. Instead, AMPK and insulin may lie on distinct pathways that converge at a point upstream of these 2 gene promoters. Investigation of the pathway by which AMPK acts may therefore give insight into themechanism of action of insulin. Our results also suggest that activation of AMPK would inhibit hepatic gluconeogenesis in an insulin-independent manner and thus help to reverse the hyperglycemia associated with type 2 diabetes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 13:00:10