Hyperlipidemia in hepatic MED1 deficient mice in response to fasting

Liang Bai, Tao Fu, Yuzhi Jia, Jayme Borensztajn, Janardan K. Reddy, Gongshe Yang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


MED1 is a key transcription co-activator subunit of the Mediator complex that is essential for RNA polymerase II-dependent transcription. MED1 functions as a co-activator for PPARs and other nuclear receptors and transcription factors, and plays an important role in lipid metabolism. To examine how MED1 might affect plasma lipids, plasma triglyceride, cholesterol levels, and lipoprotein profiles, were measured in MED1ΔLiv mice fasted for 24, 48 and 72 hours. Histological changes in liver sections from MED1ΔLiv mice after 72 hours of fasting were also examined using H&E staining. There was no fat accumulation in livers of MED1ΔLiv mice compared to MED1fl/fl and PPARα-/- control mice after 72 hours of fasting. Compared with MED1fl/fl mice, plasma triglycerides in MED1ΔLiv mice were significantly increased after 24, 48 and 72 hours of fasting, and plasma cholesterol was significantly increased after 48 and 72 hours of fasting. Lipoprotein profiles were similar in fed MED1fl/fl and MED1ΔLiv mice. However, very low density lipoprotein (VLDL) was significantly increased in MED1ΔLiv mice after 24 hours of fasting. We conclude that, hyperlipidemia in MED1ΔLiv mice in response to fasting is due to the accumulation of VLDL, which suggests that MED1 plays a pivotal role in the regulation of plasma triglyceride and cholesterol levels.

Original languageEnglish (US)
Pages (from-to)1490-1498
Number of pages9
JournalShengwu Gongcheng Xuebao/Chinese Journal of Biotechnology
Issue number10
StatePublished - Oct 2011


  • Cholesterol
  • MED1
  • Triglyceride
  • Very low density lipoprotein

ASJC Scopus subject areas

  • Biotechnology
  • Applied Microbiology and Biotechnology


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