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Regulation of energy metabolism by interleukin-1-beta, but not by interleuken-6, is mediated by nitric oxide in primary cultured rat hepatocytes

Regulation of energy metabolism by interleukin-1-beta, but not by interleuken-6, is mediated by nitric oxide in primary cultured rat hepatocytes

Biochimica et Biophysica Acta 1311(1): 20-26

The effects of inflammatory cytokines (interleukin-1-beta, interleukin-6, and tumor necrosis factor-alpha) on energy metabolism were studied in primary cultured rat hepatocytes. Adenine nucleotide (ATP, ADP, and AMP) content, lactate production, the ketone body ratio (acetoacetate/p-hydroxybutyrate) reflecting the liver mitochondrial redox state (NAD+/NADH), and nitric oxide formation were measured. Insulin increased ATP content in hepatocytes and had a maximal effect after 8-12 h of culture. Both interleukin-1-beta and interleukin-6, but not tumor necrosis factor-alpha, significantly inhibited the ATP increase time- and dose-dependently. Interleukin-1-beta and interleukin-6 also stimulated lactate production. During the same period, interleukin-1-beta but not interleukin-6 decreased the ketone body ratio. Furthermore, interleukin-1-beta markedly stimulated nitric oxide formation in hepatocytes, and this increase was blocked by N-G-monomethyl-L-arginine (a nitric oxide synthase inhibitor) and by interleukin-1 receptor antagonist. N-G-monomethyl-L-arginine reversed inhibition of the ATP increase, decrease in the ketone body ratio, and increase in lactate production, which were induced by interleukin-1-beta. Interleukin-1 receptor antagonist completely abolished all of the effects induced by interleukin-1-beta. These results demonstrated that interleukin-1-beta and interleukin-d affect the insulin-induced energy metabolism in rat hepatocytes by different mechanisms. Specifically, interleukin-1-beta inhibits ATP synthesis by causing the mitochondrial dysfunction, a process which may be mediated by nitric oxide.

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Accession: 009321432

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PMID: 8603098

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