Supplemental Figure Legends
Fig. S1. Effects of high fat diet on body weight, liver triglyceride level, and expression of hepatic
lipogenic genes. (A) Summary of animal profiles used for ChIP-seq analysis. Mice were fed normal or
high fat chow for 20 weeks and body weight s were monitored. Statistical significance was determined
by the Student’s t-test (SEM, n=3, 4). (*,p<0.01). Mice were fed normal or high fat chow for 20 weeks
and oil-red staining of liver sections was performed (B) and mRNA levels of genes involved in hepatic
lipogenesis were measured by q-RTPCR (C). Statistical significance was determined by the Student’s
t-test (SEM, n=3). (*,p<0.05).
Fig. S2. Effects of high fat diet on expression of endogenous FXR. Mice were fed normal or high
fat chow for 16 weeks and livers were collected for measuring protein (A, B) and mRNA levels (C) of
FXR. Statistical significance was determined by the Student’s t-test (SEM, n=3 for normal mice, n=4 for
dietary obese mice). (*,p<0.01, NS, statistically not significant).
Fig. S3. Supplemental information for detailed experimental procedures.
ChIP assays:
Liver tissue from mice was collected, and proteins and DNA were cross-linked with 1% formaldehyde in
PBS at room temperature for 10 min. Cross-linking was stopped by adding 125 mM glycine followed by
washing the tissue twice with ice-cold PBS. The tissues were resuspended in hypotonic buffer (10 mM
HEPES, pH 7.9, 1.5 mM MgCl2, 10 mM KCl, 0.2% NP40, 0.15 mM spermine, 0.5 mM spermidine, 1
mM EDTA, 5% sucrose) and cells were broken by Dounce homogenization and nuclei were isolated by
centrifugation. The nuclei were resuspended in sonication buffer (50 mM Tris-HCl, pH 8.0, 2 mM EDTA,
1% SDS) and sonicated to reduce the DNA length to 200-800 bp. After centrifugation, the supernatant
was diluted, pre-cleared by incubation with a 25% protein G-Sepharose slurry at 4oC for 30 min, and
chromatin was immunoprecipitated with 1-2 microgram of antibodies to FXR (Santa Cruz, H130 and
C20) or IgG as a negative control, at 4oC overnight. The immune complexes were collected by
incubation with 50 microliter of a 25% protein G Sepharose slurry for 1 h and the beads were washed
extensively with low salt, high salt, and LiCl wash buffers followed by washing twice with Tris-EDTA
(TE) buffer. After the elution of bound chromatin, the genomic DNA was purified by phenol-chloroform
extraction and subjected to PCR or qPCR using primers specific for the Shp and Ost beta promoter
region which are known to contain a FXR binding region or the Gapdh promoter as a negative control.
Deep sequencing of ChIP-DNAs and genomic mapping of DNA reads:
Twenty ng of DNA from chromatin that had been immunoprecipitated by FXR antibody, or IgG
(negative control) in samples from normal or obese mice were used for ChIP-seq library construction
(Illumina). Deep sequencing was then done using the Illumina/Solexa Genome Analyzer II
(Biotechonology Center, UIUC). Fully sequenced ChIP-DNA (50 bp) was used for genome alignment
with Mus musculus genome sequences, NCBI m37 genome assembly (mm9: July 2007) as a reference
sequence, allowing 2 bp mismatches. Sequences aligned to the mouse genome sequence were
subjected to analysis with CisGenome (v1.2) to generate FXR binding site peaks using a false
discovery rate (FDR) cutoff ( <0.001). For the FXR peak identification in the GW4064-treated samples,
two criteria such as FDR (<0.001) and ratio (>5) of FXR binding to IgG peaks were used in both diet
groups to detect binding sites.
Gene Annotation and Gene Ontology (GO) analysis:
FXR binding sites (15,263 and 5,272) in normal or high fat diet samples were analyzed to identify the
gene locations of the sites in the mouse genome. A list of all genes with FXR peaks within ± 10 kb of
the genes was generated using CisGenome. Annotated genes near FXR binding sites uniquely
detected in either the normal or high fat groups were 2,583 or 1,566, respectively. GO analysis of FXR
target genes was conducted by using the NIH database for Annotation, Visualization, and Integrated
Discovery (DAVID: http://david.acc.ncifcrf.gov/) for functional grouping of binding genes. This analysis
was also used to classify the genes into functionally related groups by using PANTHER biological
process terms (http://www.pantherdb.org). All sequence analyses were conducted based on the Mus
musculus NCBI m37 genome assembly (mm9:July 2007) accessed from Ensemble. Enrichment scores
and P-values were also generated by this analysis.
Motif search:
The enrichment of motifs within the 250 top scoring FXR binding peaks, with exception of simple
repeats in the ChIP-seq data of ND or HFD fed groups was analyzed in MEME (Multiple Em for Motif
Elicitation; http://www.meme.sdsc.edu) as position dependent letter-probability matrices. The
coordinates of each peak are set to collect motif lengths of 6 to 20 bp. Comparison of motifs against a
database of known FXRE’s was done in TOMTOM generating p-values of the similarity score, scoring
details and a logo alignment for each match.
Fig. S4. List of mouse gene primer sequences for ChIP (A) and q-RTPCR (B) analyses.
Fig.S5. GW4064 treatment resulted in increased FXR binding at known target genes. Normal or
high fat dietary obese mice were injected i.p with vehicle or GW4064 and after 1 h livers were collected.
(A) Relative occupancies of FXR at the Shp and Ostgene were determined by ChIP assays using
FXR antibody and control IgG. FXR binding in vehicle-treated normal mice was set to 1. (B) The
mRNA levels of the Shp gene were determined by q-RTPCR. Three independent ChIP assays were
done in mouse liver and genomic DNA was pooled and analyzed by genomic sequencing.
Fig.S6. Identification of genome-wide FXR binding sites by ChIP-seq. The numbers of total reads
and FXR binding sites in vehicle or GW4064-treated normal (ND) and high fat diet-induced obese
(HFD) mice are shown.
Fig. S7. Validation of binding of ligand-activated FXR in normal mice. Normal mice were treated
with GW4064 for 1 h and livers were collected for ChIP assays. Occupancies of FXR at randomly
selected genes were examined by ChIP assays. Genomic DNA from 3 independently performed ChIP
assays were pooled and used for the q-PCR analysis. FXR binding in vehicle-treated normal mice was
set to 1.
Fig. S8. Validation of binding of ligand-activated FXR in obese mice. Dietary obese mice were
treated with GW4064 for 1 h and livers were collected for ChIP assays. Occupancies of FXR at
randomly selected genes were examined by ChIP assays. Genomic DNA from 3 independently
performed ChIP assays were pooled and used for the q-PCR analysis. FXR binding in vehicle-treated
obese mice was set to 1.
Fig. S9. A list of potential FXR target genes with binding sites uniquely in the 5’ UTR or 3’UTR of
normal or obese mice. Gene name, reference sequence ID, binding site distance to TSS, and binding
site distance to TES are shown.
Genes with their 5’UTR bound by FXR uniquely in ND condition
Gene name
Refseq_ID
Binding site distance to TSS Binding site distance to TES
Npc1
NM_008720
6
-46686
Fabp1
NM_017399
7
-5128
5730559C18Rik
NM_028872
7
-20726
Htra2
NM_019752
12
-3277
Igfbp2
NM_008342
20
-27948
Tmem37
NM_019432
43
-6360
2210021J22Rik
NM_197998
46
-4641
Rev1
NM_019570
46
-76830
Glul
NM_008131
49
-9720
Rnf113a2
NM_025525
75
-1303
Pdcd6
NM_011051
102
-14103
Adam19
Aoah
Aip
Relt
Smcr7
Zscan22
Dpysl3
Ccdc85a
Lrrc27
Smap1l
Spata22
Mbd6
B3galnt1
Ltb4r1
Herc4
Myom3
Cebpg
4933421E11Rik
Inpp5e
Aldh3a1
Tnk2
Trim21
Ube2i
Zfp750
Bdh2
Hps1
Rem2
6430514L14Rik
Cntn4
Yipf1
Btbd16
U46068
Trpv2
Tdg
Trim6
Zmym3
Chrm4
Nfrkb
Stx7
Golm1
Otop2
Anxa11
Tjp2
Dppa1
Ascc2
Zfhx4
NM_009616
NM_012054
NM_016666
NM_177073
NM_001009927
NM_001001447
NM_009468
NM_181577
NM_027164
NM_133716
NM_001045531
NM_033072
NM_020026
NM_008519
NM_026101
NM_001085509
NM_009884
NM_028081
NM_033134
NM_001112725
NM_001110147
NM_001082552
NM_011665
NM_178763
NM_027208
NM_019424
NM_080726
NM_029784
NM_173004
NM_145550
NM_001081038
NM_001012392
NM_011706
NM_011561
NM_001013616
NM_019831
NM_007699
NM_172766
NM_016797
NM_001035122
NM_172801
NM_013469
NM_011597
NM_178247
NM_029291
NM_030708
Genes with their 3’UTR bound by FXR uniquely in ND condition
103
156
210
211
221
229
280
332
388
393
396
434
435
465
488
526
550
560
599
610
612
792
823
1029
1069
1075
1092
1101
1173
1211
1262
1294
1390
1539
1635
1669
1694
1935
1955
2067
2292
2302
2311
2335
2345
2350
-91252
-229977
-11171
-17354
-4332
-10195
-68769
-195149
-29597
-48529
-15907
-6381
-24240
-2065
-73404
-55323
-9594
-14334
-12340
-9064
-38238
-6755
-12957
-7295
-22064
-23705
-3242
-51146
-995352
-44180
-50566
-28231
-24429
-18854
-14722
-14795
-5946
-33186
-37687
-38721
-22848
-42347
-128141
-18473
-43247
-194951
Gene name
Klhl26
Stx5a
Atp7b
Acbd4
Plcl2
C130026I21Rik
Sepx1
Ncoa5
Emilin1
Onecut3
Flnb
Inadl
Abtb1
Cyb5b
Scamp1
Upk1a
Ablim3
C130057D23Rik
D11Wsu99e
Cacna2d2
Ncoa3
Refseq_ID
NM_172052
NM_019829
NM_007511
NM_001081495
NM_013880
NM_001037909
NM_013759
NM_144892
NM_133918
NM_139226
NM_134080
NM_001005787
NM_030251
NM_025558
NM_029153
NM_026815
NM_198649
NM_177818
NM_138598
NM_020263
NM_008679
Binding site distance to TSS Binding site distance to TES
26710
-12
13806
-16
65689
-37
10422
-89
178957
-96
24111
-111
5942
-194
34219
-203
7282
-205
22140
-214
133400
-230
142139
-237
5678
-272
36528
-281
83567
-281
8977
-405
111990
-415
9755
-438
22378
-454
128993
-470
80132
-473
Genes with their 5’UTR bound by FXR uniquely in HFD condition
Gene name
Refseq_ID
Binding site distance to TSS Binding site distance to TES
Pcyox1l
NM_172832
6
-10792
Ptgds2
NM_019455
374
-24992
Ubxd3
NM_178671
424
-18205
Atp6v1c2
NM_133699
527
-39464
Pkm2
NM_011099
890
-21877
Enpp5
NM_032003
1040
-6650
C330021F23Rik
NM_001024728
1242
-15536
Clcn4-2
NM_011334
1542
-15653
Cep164
NM_001081373
1573
-60119
Vasn
NM_139307
1697
-9096
P2ry14
NM_001008497
1868
-14131
Oma1
NM_025909
1983
-50599
Pigr
NM_011082
2407
-27061
Zfp78
NM_001025163
2693
-16607
Genes with their 3’UTR bound by FXR uniquely in HFD condition
Gene name
Refseq_ID
Binding site distance to TSS Binding site distance to TES
EG546166
NM_001024730
2813
-53
Cma2
NM_001024714
2498
-69
Fig. S10. Distribution of FXR binding sites near the TSS. Distances from the center of each FXR
binding peaks to the TSS are shown for GW4064-treated normal and high fat diet-induced obese mice.
Fig. S11. Effects of GW4064 on FXR binding sites unique to either normal or obese mice by
ChIP-seq. ChIP-seq data showing FXR binding sites in vehicle- or GW4064-treated normal and obese
mice are displayed using the UCSC genome browser. Chromosomal locations are shown at the top of
each display. The Y-axis shows the number of mapped sequence tags. Gene positions are indicated
at the bottom of each display with the arrows indicating the transcriptional start site.
Fig. S12. Effects of GW4064 treatment on mRNA levels of potential FXR target genes. Normal
mice were treated with vehicle or GW4064 for a short time, 1 h, to examine direct effects of GW4064 on
expression of potential FXR target genes. The mRNA levels of genes nearest to FXR binding sites that
were unique to normal mice were determined by q-RTPCR. Statistical significance was determined by
the Student’s t test from 11q-RTPCR readings from 4 mice (SEM, n=11).
Supplemental Information
Fig. S1A
Condition
Group of mice
Diet
Fig. S1B
ND
HFD
Number of mice
4
4
3
4
Body weight
(g, mean± SEM)
29.02
± 1.28
31.35
± 0.63
35.75
± 0.53**
35.47
± 1.01**
Ages
(month,
mean± SD)
7.7 ± 2.6
8.5 ± 1.3
9.5 ± 0.7
8.5 ± 1.3
GW4064
(30mg/Kg/day)
-
+
-
+
Oil Red Staining
Q-RTPCR
HFD
Rel mRNA Level
ND
A
*
2
0
ND
HFD
WB: FXR Ab
WB: Lamin Ab
B
HFD
FXR protein
level
NS
1.5
Rel mRNA level
1.5
C
1.0
FXR mRNA
level
*
1
0.5
0.5
0
0.0
ND
HFD
p=0.07
20
10
1
50
ND
SCD1
30
Kd
Relative protein level
Fig. S2
SREBP-1c
3
ND
HFD
0
ND
HFD
Fig. S3 Supplemental information for detailed experimental procedures
Fig. S4A.
List of primer sequences for ChIP-qPCR
No.
Gene
Forward (5’-3’)
Reverse (5’-3’)
No.
Gene
Forward (5’-3’)
Reverse (5’-3’)
1
Ostα
ATGCACGTGTGTCTGTGTGT
GCACACGCATTTGCATAGAC
32
Pklr
ACACACACACACACCCCAAG
AGGGCTTCATGCACACTAGG
2
Ostβ
ATGCATGACCTCCAGTGACA
GCAGATCATACTGGGCTCCT
33
Casp6
GTGCAGTGAAGGACGTAGCA
AGTTTAAACAGCCGGGAAGC
3
Pltp
GTCTCCAGGCTGTCTGGTTC
TGTGCTGGGGTAAAGGTAGC
34
Bcl3
AGAGTGGAGCGTCCTGTTGT
TTCCTGTGTAGTGGGTGAGC
4
Tm9sf1
GCACGGACCGGTTATTGTT
AGGGTGAAATGGCAAACTGT
35
Esr2
ATGCACGTGTGTCTGTGTGT
GCACACGCATTTGCATAGA
5
Ptma
GAAGGTGCGAGTCACAGTCA
CGCACCGAAGAGCAAGTT
36
Il2rb
AGGGCGTGCCTCTAGCTATT
GCATCTTTCTCGGGCTTCTA
6
Cyp8b1
TTTGGAGTAAGGGCATCGAG
GGCTCACCCACACTTGACTC
37
Foxo4
GGGCCAGACTGAACAGAAGA
GATTGTGGCATGGCAGTCTA
7
Atg3
CGAGGTTCGATGCCAGTC
CGGAGGGACTGTCGCAAT
38
Oxct2b
GTGTGTGTGTACACGTGCTCT
CTGCCCAGCTCTGGATAGAA
8
Nr1i3
TGGTATGAGGTGTGGAGCAA
GTGGAGGATCGACTCCAAAA
39
Slc7a15
GCATCCCTCATATTCCATGT
TGTGGAGGCACTGTAGAGCA
9
Man2c1
GAACAAAGTTCCCGCCACT
AAACGCTCTCCCTTGGCTA
40
Aldh1l2
AACTAGGCTGGCCTTGAACTC
GGTGGTGCATGCCTTTAATC
10
Ppp2cb
TGTCATTCTTCGGTGGATCA
ACAGCGCCATACAGTGAACA
41
Pgm2l1
CCACGCACATACACATACCAC
TCCTGGATGTGGCACACTAA
11
Map3k13
TGTTAGCTCAGGCACAGGAA
GAGACAGGGTCTTGCGTAGC
42
Man1b1
CAAGTCATGGGGATTTCAGG
CATCCCATACATGGCACAAG
12
Hlf
CAGTGGTTTCTACCTGTTGTC
CTGCCCTGTCACATTCCTCT
43
Gcnt7
AAGGCCAATTCTCCTTCCAT
TCTGTCAGGCCAGTGAGATG
13
Gcnt7
AAGGCCAATTCTCCTTCCAT
TCTGTCAGGCCAGTGAGATG
44
Guca1a
CTGGATGCTCCAACCCTTTA
TCCAGTAAGGAGCGAAAGGA
14
Tnfsf4
AAATTTTGGTGCATGTGTGTG
GCCAAGCCTGATAACCTGAG
45
Sc5d
CATTCATACAAACATGCACACAG
CCACGCGGATTCATTTTT
15
Art2b
GTGGACAGTGCCTGAGTGAA
CACCTACTCATGCGTGTGCT
46
Tnfsf4
AAATTTTGGTGCATGTGTGTG
GCCAAGCCTGATAACCTGAG
16
Man1a
ATCTTTGGAAAAAGGGCAAA
TGGGGTGTAAGCATGTGTGT
47
Esrrb
TGGATGGATGAGTGTGTGTG
ACCTGTCACGTCAATGACCA
17
Plau
GTTGCAGTGACTGACCCTTG
ACACATGCACACATGCACAC
GTCCACATGGCATGGACAG
Pcdhgc4
Mas1
GCGGGTATGTGTATGTGTGTTT
18
48
CACCCCATATACCCCACAGA
CCCATGTGGAATGTGTGTGT
19
Pigr
CCCTGCAGTGCATCAGAGT
ACACACACTCCACATACATGCT
49
Atg2a
ACCTCGTGTGACTGTTGCTG
GTCCTTCCCTAAACCCAAGC
20
Hic2
TTAGAAGAGGGGTGGGCATA
CTAGCATGGTGTCCAGAGCA
50
Ppp2r5c
CTCCCCGTAAAACCTGAACA
GAGGGTGAATGTCCAAGGAA
21
Hif1a
GCCATGGAGATGGAAATGAC
TCAGTACCACCCAAACCAAA
51
Ptprf
ACCTACGGCAGCTGATGAAC
GAGGTGGGAAAGACAGACCA
52
Cdca4
GGTCAGCATGAGACAAAGCA
GTGGCACCATTAGGAGGTGT
53
Musk
TTTTGTTTGTGTGTGGGTTG
GCATGTCTCAAACAATAAGGTGA
22
Mettl1
TGTGGGGTGTGTGTATGGTG
TTGAAGGGAAGGCTTTACACA
23
Aldh2
TCCCTCAGGTACCAGGAATG
CAACTGTCAGGAAAGGAACCA
24
Cma2
GCGTGCATCAGAGTCTTCAA
GGACATGCTAGGGACATGCT
54
Cma2
GCGTGCATCAGAGTCTTCAA
GGACATGCTAGGGACATGCT
25
Wnt5a
AGTGTGCACGAGGGTGTGTA
CCAGGCTGCAAAGGTTTAGA
55
Hic2
TTAGAAGAGGGGTGGGCATA
CTAGCATGGTGTCCAGAGCA
26
Map2k1
AAAGGAAACAGCATGTGCAA
CCCCTCCCTTCTCTAACCAC
56
Pla1a
CATTTGTTTGGTTGCTGGTG
GCTGCAGGGTAGGACTGAAG
27
Adh7
CTCTCTCCTTCCCCACCAC
ATGGCAAATACACAGGCACA
57
Ugdh
CAAGGCGTATGCAACGTAGA
GGGACAGTTCGGTGGTAGAG
28
Nos1
GGCTTTGGAGGAGAGGAGAA
GATGGGTTGGAGGTTAGCAA
58
Scarb2
CCTTAGTACCGCCAGGAATG
GATGCACCTTGCTCCTCTTC
29
Il2ra
TCACTAAGTCATTTCTCCAGACC
CACACACACACGATGCATTT
59
Mettl1
AGGGCTGTTTGAACCTAGCA
TGTCCCCTTCCTTAGGGACT
30
Slc2a3
AGGTCTCACATCGCAGCTCT
GGTTACCCGAAAGACAGCAG
60
Ppp1r13b GACCCCCAGAGAACTCATCA
CCATTTGTGCCTGACACTTG
31
Tmem93
GCTGCCTCGCTGATGAAC
CTCGGTTTTCTCCACAGCTC
61
Map2k5
GTTCCCAGAGCCCATGTAGA
GCTACCTGATCCCACAAGGA
Fig. S4B. List of primer sequences for q-RTPCR
No.
Gene
Forward (5’-3’)
Reverse (5’-3’)
1
Musk
ccgatgtgtctgctctttga
acaggacagtggtggaggac
2
Cma2
gaaccacactcccgacctta
tgtgcagcagtcatcacaaa
3
Hic2
ctccactgtgttccagcaga
aactcaggcagctggaggta
4
Pla1a
cctaacccacagtgccagat
atgcagaccgtcttcttgct
5
Ugdh
cgcatatttgatgccaacac
tccgggttctttaggtcctt
6
Atg2a
cgcctggaacttacttgctc
tacttggcctcagtgctcct
7
Ppp2r5c
cccagaagaggatgaaccaa
tgggttggaaatctggagac
8
Ptprf
acccgatggctgagtacaac
gccttcacctgttttgggta
9
Cdca4
aggaggaaatgagccaggat
tcccctcactgtacgacaca
10
Oxct2b
cttggcgagcaactacatca
cgtcggcatctacctcattt
11
Slc7a15
tctcccccacacttacaagg
tgagcacgaacaggaagatg
12
Aldh1l2
gaggtgaacgggatgacagt
catctgtggggttgacagtg
13
Pgm2l1
agcagccagccaaataagaa
agtagcgacacagccgtttt
14
Man1b1
tgtgaacattggcactggat
ctccaactgaatgctcgtca
15
Gcnt7
ttgcgccttcatctttcttt
aagccgagcacagttcatct
16
Guca1a
gtgccgaggaattcacagat
atctggtccttctgcacacc
17
Sc5d
ctcaccacacagaccaccac
gcctccaattctatcccaca
18
Tnfsf4
ccctggatgagaatctggaa
cagagaccaccagccttagc
19
Esrrb
acacttggggaccagatgag
ctaccaggcgagagtgttcc
20
Mas1
ttggtgaccaccatggagta
gcggagtgaagaccaagaag
21
Nr0b2
cagtgagaaccctggtctt
ctggccaaacaaccttgac
22
Ostb
ccgcaatggcagatcatac
gtgaatgaccccacgaatg
Fig. S5
A
B
4
3
2
1
0
GW4064
Diet
-
+
ND
-
+
HF
mSHP levels
Rel mRNAs
5
FXR on Ostβ
Fold enrichment
Fold enrichment
FXR recruit on Shp
15
10
5
16
14
12
10
8
6
4
2
0
GW4064
Diet
0
-
+
ND
-
GW4064
Diet
+
HF
-
+
ND
-
+
HFD
Fig. S6
Mouse Diet
Normal Diet
(ND)
High Fat Diet
(HFD)
Fig. S7
12
Total number of
DNA reads
Total FXR
sites
(-GW) 5,012,745
6,923
(+GW) 2,985,933
15,263
(-GW) 6,051,048
8,387
(+GW) 3,972,513
5,272
FXR Chip-qPCR
ND+Veh
ND+GW
Fold enrichment
10
8
6
4
2
0
ta tb ltp b1 g3 i3 t7 f4 1b b2 c1 cb 13 Hlf t2b a15 2l1 a1a c5d rrb as1 t2b 1l2 r5c tprf g2a ca4
Os Os P yp8 At Nr1GcnTnfs an Nr0 an2pp2 p3k
Ar lc7 gm uc S Es M Oxc ldhpp2 P At Cd
M
A P
C
M P Ma
S P G
Fig. S8
FXR ChIP
Fold enrichment
10
Vehicle Fatty liver
GW4064 Fatty liver
8
6
4
2
Fold enrichment
0
5
4
3
2
1
0
Fig. S9. A list of potential FXR target genes with binding sites uniquely in
the 5’ UTR or 3’UTR of normal or obese mice.
Num of FXR bindings
Fig. S10
35
30
25
20
FXR unique in ND(+GW)
15
10
FXR unique in HFD(+GW)
5
0
-4000 -3000 -2000 -1000
0
1000 2000 3000 4000
Distance from TSS
Fig. S11
Scarb2-Scavenger receptor
Adh7 – Alcohol Dehydrogenase
Hlf – Hepatic Leukemia Factor
Serpinb8 – Serpin Peptidase Inhibitor
Man1b1 - Mannosidase
Pgm2l1 – Phosphoglucomutase like
Cma2 –Chymase
Foxo4 – Forkhead Box
Fig. S11
Pltp – Phospholipid Transfer Protein
Fig. S12
4
Unique FXR bindings
in ND (+GW4064)
Rel mRNA levels
ND(+GW)
ND+Veh
ND+GW (1h)
HFD(+GW)
3
2
**
1
**
**
*
*
0