Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease
Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver dysfunction, and its prevalence has markedly increased. We previously evaluated the expression of fatty acid metabolism-related genes in NAFLD and reported changes in expression that could contribute to inc...
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| Veröffentlicht in: | International journal of molecular medicine 2007-09, Vol.20 (3), p.351-358 |
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| creator | Kohjima, Motoyuki Enjoji, Munechika Higuchi, Nobito Kato, Masaki Kotoh, Kazuhiro Yoshimoto, Tsuyoshi Fujino, Tatsuya Yada, Masayoshi Yada, Ryoko Harada, Naohiko Takayanagi, Ryoichi Nakamuta, Makoto |
| description | Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes
of abnormal liver dysfunction, and its prevalence has markedly increased. We previously
evaluated the expression of fatty acid metabolism-related genes in NAFLD and reported
changes in expression that could contribute to increased fatty acid synthesis.
In the present study, we evaluated the expression of additional fatty acid metabolism-related
genes in larger groups of NAFLD (n=26) and normal liver (n=10) samples. The target
genes for real-time PCR analysis were as follows: acetyl-CoA carboxylase (ACC)
1, ACC2, fatty acid synthase (FAS), sterol regulatory element-binding protein
1c (SREBP-1c), and adipose differentiation-related protein (ADRP) for evaluation
of de novo synthesis and uptake of fatty acids; carnitine palmitoyltransferase
1a; (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), long-chain L-3-hydroxyacylcoenzyme
A dehydrogenase α (HADHα), uncoupling protein 2 (UCP2), straight-chain acyl-CoA
oxidase (ACOX), branched-chain acyl-CoA oxidase (BOX), cytochrome P450 2E1 (CYP2E1),
CYP4A11, and peroxisome proliferator-activated receptor (PPAR)α for oxidation
in the mitochondria, peroxisomes and microsomes; superoxide dismutase (SOD), catalase,
and glutathione synthetase (GSS) for antioxidant pathways; and diacylglycerol
O-acyltransferase 1 (DGAT1), PPARγ, and hormone-sensitive lipase (HSL) for triglyceride
synthesis and catalysis. In NAFLD, although fatty acids accumulated in hepatocytes,
their de novo synthesis and uptake were up-regulated in association with increased
expression of ACC1, FAS, SREBP-1c, and ADRP. Fatty acid oxidation-related genes,
LCAD, HADHα, UCP2, ACOX, BOX, CYP2E1, and CYP4A11, were all overexpressed, indicating
that oxidation was enhanced in NAFLD, whereas the expression of CTP1a and PPARα
was decreased. Furthermore, SOD and catalase were also overexpressed, indicating
that antioxidant pathways are activated to neutralize reactive oxygen species
(ROS), which are overproduced during oxidative processes. The expression of DGAT1
was up-regulated without increased PPARγ expression, whereas the expression of
HSL was decreased. Our data indicated the following regarding NAFLD: i) increased
de novo synthesis and uptake of fatty acids lead to further fatty acid accumulation
in hepatocytes; ii) mitochondrial fatty acid oxidation is decreased or fully activated;
iii) in order to complement the function of mitochondria (β-oxidation), peroxisomal
(β-oxidation) and m |
| doi_str_mv | 10.3892/ijmm.20.3.351 |
| format | Article |
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of abnormal liver dysfunction, and its prevalence has markedly increased. We previously
evaluated the expression of fatty acid metabolism-related genes in NAFLD and reported
changes in expression that could contribute to increased fatty acid synthesis.
In the present study, we evaluated the expression of additional fatty acid metabolism-related
genes in larger groups of NAFLD (n=26) and normal liver (n=10) samples. The target
genes for real-time PCR analysis were as follows: acetyl-CoA carboxylase (ACC)
1, ACC2, fatty acid synthase (FAS), sterol regulatory element-binding protein
1c (SREBP-1c), and adipose differentiation-related protein (ADRP) for evaluation
of de novo synthesis and uptake of fatty acids; carnitine palmitoyltransferase
1a; (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), long-chain L-3-hydroxyacylcoenzyme
A dehydrogenase α (HADHα), uncoupling protein 2 (UCP2), straight-chain acyl-CoA
oxidase (ACOX), branched-chain acyl-CoA oxidase (BOX), cytochrome P450 2E1 (CYP2E1),
CYP4A11, and peroxisome proliferator-activated receptor (PPAR)α for oxidation
in the mitochondria, peroxisomes and microsomes; superoxide dismutase (SOD), catalase,
and glutathione synthetase (GSS) for antioxidant pathways; and diacylglycerol
O-acyltransferase 1 (DGAT1), PPARγ, and hormone-sensitive lipase (HSL) for triglyceride
synthesis and catalysis. In NAFLD, although fatty acids accumulated in hepatocytes,
their de novo synthesis and uptake were up-regulated in association with increased
expression of ACC1, FAS, SREBP-1c, and ADRP. Fatty acid oxidation-related genes,
LCAD, HADHα, UCP2, ACOX, BOX, CYP2E1, and CYP4A11, were all overexpressed, indicating
that oxidation was enhanced in NAFLD, whereas the expression of CTP1a and PPARα
was decreased. Furthermore, SOD and catalase were also overexpressed, indicating
that antioxidant pathways are activated to neutralize reactive oxygen species
(ROS), which are overproduced during oxidative processes. The expression of DGAT1
was up-regulated without increased PPARγ expression, whereas the expression of
HSL was decreased. Our data indicated the following regarding NAFLD: i) increased
de novo synthesis and uptake of fatty acids lead to further fatty acid accumulation
in hepatocytes; ii) mitochondrial fatty acid oxidation is decreased or fully activated;
iii) in order to complement the function of mitochondria (β-oxidation), peroxisomal
(β-oxidation) and microsomal (ω-oxidation) oxidation is up-regulated to decrease
fatty acid accumulation; iv) antioxidant pathways including SOD and catalase are
enhanced to neutralize ROS overproduced during mitochondrial, peroxisomal, and
microsomal oxidation; and v) lipid droplet formation is enhanced due to increased
DGAT expression and decreased HSL expression. Further studies will be needed to
clarify how fatty acid synthesis is increased by SREBP-1c, which is under the
control of insulin and AMP-activated protein kinase.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.20.3.351</identifier><identifier>PMID: 17671740</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Antioxidants - metabolism ; Base Sequence ; Case-Control Studies ; DNA Primers - genetics ; Fatty Acids - metabolism ; Fatty Liver - genetics ; Fatty Liver - metabolism ; Gene Expression ; Humans ; Lipid Metabolism - genetics ; Male ; Mitochondria, Liver - metabolism ; Models, Biological ; Oxidation-Reduction ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>International journal of molecular medicine, 2007-09, Vol.20 (3), p.351-358</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432t-5b292a73b2a0dccc5fa677c0cf2b68e08218fa18d680045e5c86b95bd12473e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17671740$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kohjima, Motoyuki</creatorcontrib><creatorcontrib>Enjoji, Munechika</creatorcontrib><creatorcontrib>Higuchi, Nobito</creatorcontrib><creatorcontrib>Kato, Masaki</creatorcontrib><creatorcontrib>Kotoh, Kazuhiro</creatorcontrib><creatorcontrib>Yoshimoto, Tsuyoshi</creatorcontrib><creatorcontrib>Fujino, Tatsuya</creatorcontrib><creatorcontrib>Yada, Masayoshi</creatorcontrib><creatorcontrib>Yada, Ryoko</creatorcontrib><creatorcontrib>Harada, Naohiko</creatorcontrib><creatorcontrib>Takayanagi, Ryoichi</creatorcontrib><creatorcontrib>Nakamuta, Makoto</creatorcontrib><title>Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes
of abnormal liver dysfunction, and its prevalence has markedly increased. We previously
evaluated the expression of fatty acid metabolism-related genes in NAFLD and reported
changes in expression that could contribute to increased fatty acid synthesis.
In the present study, we evaluated the expression of additional fatty acid metabolism-related
genes in larger groups of NAFLD (n=26) and normal liver (n=10) samples. The target
genes for real-time PCR analysis were as follows: acetyl-CoA carboxylase (ACC)
1, ACC2, fatty acid synthase (FAS), sterol regulatory element-binding protein
1c (SREBP-1c), and adipose differentiation-related protein (ADRP) for evaluation
of de novo synthesis and uptake of fatty acids; carnitine palmitoyltransferase
1a; (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), long-chain L-3-hydroxyacylcoenzyme
A dehydrogenase α (HADHα), uncoupling protein 2 (UCP2), straight-chain acyl-CoA
oxidase (ACOX), branched-chain acyl-CoA oxidase (BOX), cytochrome P450 2E1 (CYP2E1),
CYP4A11, and peroxisome proliferator-activated receptor (PPAR)α for oxidation
in the mitochondria, peroxisomes and microsomes; superoxide dismutase (SOD), catalase,
and glutathione synthetase (GSS) for antioxidant pathways; and diacylglycerol
O-acyltransferase 1 (DGAT1), PPARγ, and hormone-sensitive lipase (HSL) for triglyceride
synthesis and catalysis. In NAFLD, although fatty acids accumulated in hepatocytes,
their de novo synthesis and uptake were up-regulated in association with increased
expression of ACC1, FAS, SREBP-1c, and ADRP. Fatty acid oxidation-related genes,
LCAD, HADHα, UCP2, ACOX, BOX, CYP2E1, and CYP4A11, were all overexpressed, indicating
that oxidation was enhanced in NAFLD, whereas the expression of CTP1a and PPARα
was decreased. Furthermore, SOD and catalase were also overexpressed, indicating
that antioxidant pathways are activated to neutralize reactive oxygen species
(ROS), which are overproduced during oxidative processes. The expression of DGAT1
was up-regulated without increased PPARγ expression, whereas the expression of
HSL was decreased. Our data indicated the following regarding NAFLD: i) increased
de novo synthesis and uptake of fatty acids lead to further fatty acid accumulation
in hepatocytes; ii) mitochondrial fatty acid oxidation is decreased or fully activated;
iii) in order to complement the function of mitochondria (β-oxidation), peroxisomal
(β-oxidation) and microsomal (ω-oxidation) oxidation is up-regulated to decrease
fatty acid accumulation; iv) antioxidant pathways including SOD and catalase are
enhanced to neutralize ROS overproduced during mitochondrial, peroxisomal, and
microsomal oxidation; and v) lipid droplet formation is enhanced due to increased
DGAT expression and decreased HSL expression. Further studies will be needed to
clarify how fatty acid synthesis is increased by SREBP-1c, which is under the
control of insulin and AMP-activated protein kinase.</description><subject>Antioxidants - metabolism</subject><subject>Base Sequence</subject><subject>Case-Control Studies</subject><subject>DNA Primers - genetics</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Liver - genetics</subject><subject>Fatty Liver - metabolism</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Lipid Metabolism - genetics</subject><subject>Male</subject><subject>Mitochondria, Liver - metabolism</subject><subject>Models, Biological</subject><subject>Oxidation-Reduction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkUtLw0AURgdRbK0u3UpWbiR1HplHliK-oCBIF-7CZOZGpySZmkmK_fdOaKSrey-c71uci9A1wUumcnrvNk2zpPFYMk5O0JzInKQ0yz5P406wTJnkYoYuQthgTHmWq3M0I1JIIjM8R-UHpLDT9aB759vEV0ml-36faONs0kCvS1-70KQd1LoHm3xBCwn8bjsIYQy4Nml9q2vjvyNopnTtdtAl1gXQAS7RWaXrAFfTXKD189P68TVdvb-8PT6sUpMx2qe8pDnVkpVUY2uM4ZUWUhpsKloKBVhRoipNlBUK44wDN0qUOS8toZlkwBbo9lC77fzPAKEvGhcM1LVuwQ-hEIqQmBQRTA-g6XwIHVTFtnON7vYFwcXotBidFjQeRXQa-ZupeCgbsEd6khiBuwMQtrq1zvpwZP4_QDEbu7hif3ebgcE</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>Kohjima, Motoyuki</creator><creator>Enjoji, Munechika</creator><creator>Higuchi, Nobito</creator><creator>Kato, Masaki</creator><creator>Kotoh, Kazuhiro</creator><creator>Yoshimoto, Tsuyoshi</creator><creator>Fujino, Tatsuya</creator><creator>Yada, Masayoshi</creator><creator>Yada, Ryoko</creator><creator>Harada, Naohiko</creator><creator>Takayanagi, Ryoichi</creator><creator>Nakamuta, Makoto</creator><general>D.A. Spandidos</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070901</creationdate><title>Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease</title><author>Kohjima, Motoyuki ; Enjoji, Munechika ; Higuchi, Nobito ; Kato, Masaki ; Kotoh, Kazuhiro ; Yoshimoto, Tsuyoshi ; Fujino, Tatsuya ; Yada, Masayoshi ; Yada, Ryoko ; Harada, Naohiko ; Takayanagi, Ryoichi ; Nakamuta, Makoto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432t-5b292a73b2a0dccc5fa677c0cf2b68e08218fa18d680045e5c86b95bd12473e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antioxidants - metabolism</topic><topic>Base Sequence</topic><topic>Case-Control Studies</topic><topic>DNA Primers - genetics</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Liver - genetics</topic><topic>Fatty Liver - metabolism</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Lipid Metabolism - genetics</topic><topic>Male</topic><topic>Mitochondria, Liver - metabolism</topic><topic>Models, Biological</topic><topic>Oxidation-Reduction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kohjima, Motoyuki</creatorcontrib><creatorcontrib>Enjoji, Munechika</creatorcontrib><creatorcontrib>Higuchi, Nobito</creatorcontrib><creatorcontrib>Kato, Masaki</creatorcontrib><creatorcontrib>Kotoh, Kazuhiro</creatorcontrib><creatorcontrib>Yoshimoto, Tsuyoshi</creatorcontrib><creatorcontrib>Fujino, Tatsuya</creatorcontrib><creatorcontrib>Yada, Masayoshi</creatorcontrib><creatorcontrib>Yada, Ryoko</creatorcontrib><creatorcontrib>Harada, Naohiko</creatorcontrib><creatorcontrib>Takayanagi, Ryoichi</creatorcontrib><creatorcontrib>Nakamuta, Makoto</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kohjima, Motoyuki</au><au>Enjoji, Munechika</au><au>Higuchi, Nobito</au><au>Kato, Masaki</au><au>Kotoh, Kazuhiro</au><au>Yoshimoto, Tsuyoshi</au><au>Fujino, Tatsuya</au><au>Yada, Masayoshi</au><au>Yada, Ryoko</au><au>Harada, Naohiko</au><au>Takayanagi, Ryoichi</au><au>Nakamuta, Makoto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>20</volume><issue>3</issue><spage>351</spage><epage>358</epage><pages>351-358</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes
of abnormal liver dysfunction, and its prevalence has markedly increased. We previously
evaluated the expression of fatty acid metabolism-related genes in NAFLD and reported
changes in expression that could contribute to increased fatty acid synthesis.
In the present study, we evaluated the expression of additional fatty acid metabolism-related
genes in larger groups of NAFLD (n=26) and normal liver (n=10) samples. The target
genes for real-time PCR analysis were as follows: acetyl-CoA carboxylase (ACC)
1, ACC2, fatty acid synthase (FAS), sterol regulatory element-binding protein
1c (SREBP-1c), and adipose differentiation-related protein (ADRP) for evaluation
of de novo synthesis and uptake of fatty acids; carnitine palmitoyltransferase
1a; (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), long-chain L-3-hydroxyacylcoenzyme
A dehydrogenase α (HADHα), uncoupling protein 2 (UCP2), straight-chain acyl-CoA
oxidase (ACOX), branched-chain acyl-CoA oxidase (BOX), cytochrome P450 2E1 (CYP2E1),
CYP4A11, and peroxisome proliferator-activated receptor (PPAR)α for oxidation
in the mitochondria, peroxisomes and microsomes; superoxide dismutase (SOD), catalase,
and glutathione synthetase (GSS) for antioxidant pathways; and diacylglycerol
O-acyltransferase 1 (DGAT1), PPARγ, and hormone-sensitive lipase (HSL) for triglyceride
synthesis and catalysis. In NAFLD, although fatty acids accumulated in hepatocytes,
their de novo synthesis and uptake were up-regulated in association with increased
expression of ACC1, FAS, SREBP-1c, and ADRP. Fatty acid oxidation-related genes,
LCAD, HADHα, UCP2, ACOX, BOX, CYP2E1, and CYP4A11, were all overexpressed, indicating
that oxidation was enhanced in NAFLD, whereas the expression of CTP1a and PPARα
was decreased. Furthermore, SOD and catalase were also overexpressed, indicating
that antioxidant pathways are activated to neutralize reactive oxygen species
(ROS), which are overproduced during oxidative processes. The expression of DGAT1
was up-regulated without increased PPARγ expression, whereas the expression of
HSL was decreased. Our data indicated the following regarding NAFLD: i) increased
de novo synthesis and uptake of fatty acids lead to further fatty acid accumulation
in hepatocytes; ii) mitochondrial fatty acid oxidation is decreased or fully activated;
iii) in order to complement the function of mitochondria (β-oxidation), peroxisomal
(β-oxidation) and microsomal (ω-oxidation) oxidation is up-regulated to decrease
fatty acid accumulation; iv) antioxidant pathways including SOD and catalase are
enhanced to neutralize ROS overproduced during mitochondrial, peroxisomal, and
microsomal oxidation; and v) lipid droplet formation is enhanced due to increased
DGAT expression and decreased HSL expression. Further studies will be needed to
clarify how fatty acid synthesis is increased by SREBP-1c, which is under the
control of insulin and AMP-activated protein kinase.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>17671740</pmid><doi>10.3892/ijmm.20.3.351</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | International journal of molecular medicine, 2007-09, Vol.20 (3), p.351-358 |
| issn | 1107-3756 1791-244X |
| language | eng |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Antioxidants - metabolism Base Sequence Case-Control Studies DNA Primers - genetics Fatty Acids - metabolism Fatty Liver - genetics Fatty Liver - metabolism Gene Expression Humans Lipid Metabolism - genetics Male Mitochondria, Liver - metabolism Models, Biological Oxidation-Reduction Reverse Transcriptase Polymerase Chain Reaction |
| title | Re-evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease |
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