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Elevated circulating and endogenous lipids increase CREBH gene expression in vivo
Author(s) -
Gentile Christopher L,
Wang Dong,
Wei Rosie,
Pagliassotti Michael J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1190.2
Subject(s) - medicine , endocrinology , endoplasmic reticulum , steatosis , messenger rna , unfolded protein response , gene expression , basal (medicine) , in vivo , insulin , chemistry , biology , gene , microbiology and biotechnology , biochemistry
CREBH is a liver‐specific transcription factor that is activated by endoplasmic reticulum (ER) stress and required for C‐reactive protein (CRP) expression. We examined whether lipids regulate CREBH and CRP gene expression in vivo. A pancreatic clamp was performed in rats in which insulin and glucose were replaced at basal levels in the absence (CON, n=5) or presence of Liposyn (LIP, n=5) infusion. Free FA were increased ~4‐fold (p<0.05) in LIP throughout the study. CREBH mRNA was increased ~3‐fold in LIP vs CON. ER stress and CRP mRNA were not increased in CON or LIP. We next examined CREBH expression in dietary models of hepatic steatosis. Rats were fed a control, high starch diet (STD, n=4) or one of two diets that produce hepatic steatosis, a high‐sucrose diet (HSD, n=4) or high fat diet (HFD, n=4) for 4 wks. CREBH mRNA was increased ~2.5 fold in HSD and HFD vs STD. ER stress and CRP mRNA were increased (~2.5 fold) in HSD only. In conclusion, CREBH gene expression is regulated by circulating and hepatic lipids and CRP is associated with hepatic ER stress. Supported by DK 072017