The Ca2+ second messenger system and interleukin-1-alpha modulation of hepatic gene transcription and mitochondrial fat oxidation.

@article{Barke1991TheCS,
  title={The Ca2+ second messenger system and interleukin-1-alpha modulation of hepatic gene transcription and mitochondrial fat oxidation.},
  author={Roderick A. Barke and Patric Brady and L J Brady},
  journal={Surgery},
  year={1991},
  volume={110 2},
  pages={285-94}
}
Cytokines have been implicated in the modulation of fat metabolism after sepsis. Carnitine palmitoyltransferase (CPT), the regulatory enzyme of hepatic mitochondrial long-chain fatty-acid oxidation, is involved in the control of hepatic fat oxidation in sepsis. Using either H4IIe rat hepatoma cells or rat hepatocytes in primary culture, we tested the hypothesis that interleukin-1-alpha (IL-1 alpha) would modulate CPT transcription (CPT mRNA), CPT translation (35S-methionine CPT protein… CONTINUE READING

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We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
We showed that either calcium ionophore ( A23187 ) or phorbol myristate acetate increased CPT gene transcription and that either calcium chelation , protein kinase C inhibition ( acridine orange ) , or chronic exposure to phorbol myristate acetate significantly inhibited IL-1 alpha induction of CPT mRNA .
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