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. 2013;36(11):1766-72.
doi: 10.1248/bpb.b13-00351.

Expression of hepatic fat-specific protein 27 depends on the specific etiology of fatty liver

Daisuke Aibara  1 , Kimihiko Matsusue, Kohei Matsuo, Soichi Takiguchi, Frank J Gonzalez, Shigeru Yamano
Affiliations

Expression of hepatic fat-specific protein 27 depends on the specific etiology of fatty liver

Daisuke Aibara et al. Biol Pharm Bull. 2013.

Abstract

Fat-specific protein 27 gene (FSP27), isolated by screening for genes specifically expressed in fully differentiated mouse adipocytes, belongs to the cell death-inducing DNA fragmentation factor, alpha subunit-like effector family. FSP27 is induced in not only adipose tissue but also the liver of ob/ob mice, and it promotes the development of fatty liver. The FSP27 gene is expressed in a fatty liver-specific manner and is not detected in the normal mouse liver. FSP27 expression is directly regulated by the induction of the hepatic peroxisome proliferator-activated receptor γ (PPARγ) in ob/ob fatty liver. In the present study, expression of hepatic FSP27 mRNA was determined in non-genetic fatty liver models. The FSP27 gene was markedly induced in the high-fat- or methionine- and choline-deficient (MCD) diet-induced fatty liver, but it was not elevated in alcohol-induced fatty liver. Interestingly, the induction of FSP27 mRNA due to the MCD diet was independent of PPARγ levels and completely absent in the liver from PPARγ-null mice. These results suggest that FSP27 mRNA expression in the liver depends on the etiology of fatty liver.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.. FSP27 Gene Expression Depends on Hepatic PPARγ Expression
QPCR analyses of FSP27 (A) and PPARγ (B) mRNAs were performed in each genotyped mouse liver. Expression was normalized to 36B4 mRNA, and each bar represents the average±S.E.M. of three separate experiments. Normal, normal genetic background mice; ob/ob, leptin-deficient mice; WT, PPARγ wild-type mice liver; KO, PPARγKO mice liver. Note: ob/ob-PPARγWT mice have fatty liver, whereas ob/ob-PPARγKO mice are normal or have much less fat. Significant differences from PPARγWT liver: * p<0.01, ** p<0.001.
Fig. 2.
Fig. 2.. FSP27 Gene Expression in Fatty Livers Developed by Different Methods
QPCR analyses of FSP27, PPARγ, aP2, and CD36 mRNAs were performed using liver samples from each group. Expression of each mRNA was examined in genetically modified (A) leptin receptor-mutated mice (db/db), as well as in mice fed diets comprising either (B) high fat (HF), (C) alcohol (AL), or (D) lacking methionine and choline (MCD). Expression was normalized to 36B4 mRNA, and each bar represents the average±S.E.M. of 3 individual experiments. Significant differences from db/m mice or control diet: * p<0.05, ** p<0.01, *** p<0.001.
Fig. 3.
Fig. 3.. Induction of FSP27 mRNA in MCD Fatty Liver Is Potentially Regulated by Hepatic PPARγ
QPCR analysis of FSP27 (A) and PPARγ (B) mRNAs were performed using liver samples from each genotyped mouse. Expression was normalized to 36B4 mRNA, and each bar represents the average±S.E.M. of 3 individual experiments. Significant differences from PPARγWT liver: * p<0.001.
Fig. 4.
Fig. 4.. Hepatic TG Content in MCD Fatty Liver Is Independent of FSP27 Levels
(A) Hepatic TG content in PPARγWT and PPARγKO mice fed a MCD diet. Each bar represents the average±S.E.M. of 3 individual experiments. (B) QPCR analysis to assess the effects of PPARγ deficiency on hepatic gene expression. QPCR analyses of FAS, SREBP1c, aP2, and PEPCK mRNAs were performed using liver samples for each genotyped mouse. Expression was normalized to 36B4 mRNA, and each bar represents the average±S.E.M. of 3 individual experiments. Note: no significant differences on all data were observed between PPARγWT and PPARγKO mice fed a MCD diet.
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