“Woah! It's like Spotify but for academic articles.”

Instant Access to Thousands of Journals for just $40/month

Get 2 Weeks Free

Inflammatory Liver Steatosis Caused by IL-12 and IL-18

Inflammatory Liver Steatosis Caused by IL-12 and IL-18

Abstract

Acute fatty degeneration in the liver is caused by various agents, such as aspirin, valproic acid, and ibuprofen, that directly inhibit mitochondrial beta-oxidation of fatty acid and oxidative phosphorylation. Endogenous molecules, such as cytokines and hormones, are also known to mediate microvesicular steatosis in liver failure. In this study, we examined how interleukin-12 (IL-12) and IL-18 cause steatosis in the liver. Administration of these cytokines in combination caused marked hepatosteatosis and weight loss in mice. There were marked increases in levels of interferon- γ (IFN- γ ), nitrite (NO 2 /NO 3 ), and fibrinogen in the circulation in these mice. On the other hand, the ATP concentration and blood flow in the liver were significantly reduced. These changes, except the production of IFN- γ and NO, were partially inhibited by Z-VAD-fmk, a synthetic tripeptide inhibitor for NO-induced caspases. These results indicate that IL-12 and IL-18 may mediate inflammatory hepatosteatosis through impairment of the microcirculation, which leads to mitochondrial dysfunction in hepatocytes.
Loading next page...
Problems Reading this Article? Report Issue Here
 
/lp/mary-ann-liebert/inflammatory-liver-steatosis-caused-by-il-12-and-il-18-g2HwAc05BD

You're reading a free preview. Subscribe to read the entire article.

And millions more from thousands of peer-reviewed journals, for only $40/month.

Get 2 Weeks Free

To be the best researcher, you need access to the best research

  • With DeepDyve, you can stop worrying about how much articles cost, or if it's too much hassle to order — it's all at your fingertips. Your research is important and deserves the top content.
  • Read from thousands of the leading scholarly journals from Springer, Elsevier, Nature, IEEE, Wiley-Blackwell and more.
  • All the latest content is available, no embargo periods.

Stop missing out on the latest updates in your field

  • We’ll send you automatic email updates on the keywords and journals you tell us are most important to you.
  • There is a lot of content out there, so we help you sift through it and stay organized.