Nitric oxide, sepsis and liver metabolism

Ceppi, E D, Smith, F S and Titheradge, M A (1997) Nitric oxide, sepsis and liver metabolism. Biochemical Society Transactions, 25 (3). pp. 929-934. ISSN 03005127

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Abstract

Treatment of rats with bacterial endotoxin (LPS) significantly lowers hepatic gluconeogenesis and induces nitric oxide (NO) synthase over 18 hours. The induction of NO synthase correlates with alterations in plasma nitrate plus nitrite, and also with an inhibition of glucose synthesis in subsequently isolated hepatocytes. Artifical NO donors similarly decrease glucose synthesis. Cultured hepatocytes treated with a mixture of LPS, interferon-¿, tumour necrosis factor-a and IL-1ß show a similar inhibition of glucose output and induction of NO synthase, although NO synthase inhibitors can only partially reverse the inhibition of glucose output. Inclusion of glucagon during the induction period diminishes the ability of the cytokines to induce NO synthase and attenuates the inhibitory effect on glucose output. The inhibitory effect of glucagon on the expression of NO synthase can be mimicked by dibutyryl cyclic AMP and forskolin.

Item Type: Article
Schools and Departments: School of Life Sciences > Biochemistry
Depositing User: Michael Titheradge
Date Deposited: 06 Feb 2012 21:15
Last Modified: 26 Mar 2012 11:37
URI: http://sro.sussex.ac.uk/id/eprint/30509
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