Supported in part by the National Institutes of Health (grants GM23750 and DK083163 to J.K.R; Clinical Nutrition Research Unit grant DK56351 to N.E.W); China Scholarship Council (to L.B.).
Steatohepatitis/Metabolic Liver Disease
Article first published online: 7 APR 2011
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 53, Issue 4, pages 1164–1174, April 2011
How to Cite
Bai, L., Jia, Y., Viswakarma, N., Huang, J., Vluggens, A., Wolins, N. E., Jafari, N., Rao, M. S., Borensztajn, J., Yang, G. and Reddy, J. K. (2011), Transcription coactivator mediator subunit MED1 Is required for the development of fatty liver in the mouse. Hepatology, 53: 1164–1174. doi: 10.1002/hep.24155
Potential conflict of interest: Nothing to report.
- Issue published online: 7 APR 2011
- Article first published online: 7 APR 2011
- Accepted manuscript online: 12 JAN 2011 10:32AM EST
- Manuscript Accepted: 16 DEC 2010
- Manuscript Received: 20 SEP 2010
- National Institutes of Health. Grant Numbers: GM23750, DK083163
- Clinical Nutrition Research Unit. Grant Number: DK56351
- China Scholarship Council
Additional Supporting Information may be found in the online version of this article.
|HEP_24155_sm_suppinfofig1.tif||2216K||Supporting Fig. 1. Med1 deficiency increases glucose tolerance and insulin sensitivity. (A-B) Glucose tolerance test (GTT) for Med1fl/fl and Med1ΔLiv after 1 month (A), and 4 months (B) of high fat diet (HFD) feeding (60% kcal fat). (C) Insulin tolerance test (ITT) for Med1fl/fl and Med1ΔLiv after 1 month of HFD treatment. *P<0.05; ** P<0.01 (D) Body weight gain of Med1fl/fl and Med1ΔLiv after 0, 1 and 4 months of HFD feeding.|
|HEP_24155_sm_suppinfofig2.tif||9682K||Supporting Fig. 2. Nuclear immunohistochemical localization of PPAR? is noticeably detected in Med1f/fl and MedΔLiv mouse liver after 5 days of Ad/ PPAR? adenofection. (Left and middle panels) Positive staining of hepatocyte nuclei in overexpressed PPAR? Med1f/fl and MedΔLiv mouse livers respectively. And (right panel) basal nuclear staining in uninjected Med1f/fl control mice.|
|HEP_24155_sm_suppinfofig3.tif||9811K||Supporting Fig. 3. Transcription coactivators SRC-1, PRIC285, PRIP, and PIMT are not necessary for PPAR? stimulated adipogenic steatosis in liver. (A) Gross photographs, H&E and Oil Red O staining for SRC−1+/+, SRC-1−/−, PRIC285fl/fl, PRIC285-/-, PRIPfl/fl, PRIPΔLiv, PIMTfl/fl and PIMTΔLiv mouse livers 5 days after Ad/LacZ or Ad/PPAR? injection and their uninjected corresponding controls. (B-E) Liver/body weight ratio of SRC−1+/+, SRC-1−/− (B), PRIC285fl/fl, PRIC285-/- (C), PRIPfl/fl, PRIPΔLiv (D), and PIMTfl/fl, PIMTΔLiv (E) mice 5 days post injection of Ad/LacZ or Ad/PPAR? (n=5), compared to their corresponding controls without injection. SRC-1−/− and PRIC285-/- represent germ line deletion, and PRIPΔLiv and PIMTΔLiv represent liver specific deletion.|
|HEP_24155_sm_suppinfofig4.tif||2044K||Supporting Fig. 4. PPAR? stimulated adipogenic gene expression in liver is unaffected by SRC-1, PRIC285, PRIP and PIMT deficiency. Expression of lipogenesis related genes in SRC−1+/+ (lanes 1-3), SRC-1−/− (lanes 4-6), PRIC285fl/fl (lanes7-9), PRIC285-/- (lanes 10-12), PRIPfl/fl (lanes 13-15), PRIPΔLiv (lanes 16-18), PIMTfl/fl (lanes 19-21) and PIMTΔLiv (lanes 22-24) mice uninjected (-), or following injection with Ad/LacZ (+) or Ad/PPAR? (+). Total RNa from 3 mice aged 5 weeks were pooled for Northern blot analysis. Names of the probes used are indicated on the right of the blot. 28S and 18S used as loading control.|
|HEP_24155_sm_suppinfotable1.doc||277K||Supporting Table 1. Genes up-regulated 4-fold or greater in MED1fl/fl mouse livers after Ad/PPARγ stimulation but not in MEDΔLiv mouse livers|
|HEP_24155_sm_suppinfotable2.doc||30K||Supporting Table 2. Specific Primers for Q-PCR|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.