Effect of Tricaprin on Cardiac Proteome in a Mouse Model for Triglyceride Deposit Cardiomyovasculopathy
Triglyceride deposit cardiomyovasculopathy (TGCV), a rare cardiovascular disorder caused by genetic or acquired dysfunction of adipose triglyceride lipase (ATGL), is marked by defective intracellular lipolysis that results in excessive accumulation of triglycerides (TGs) in the myocardium and corona...
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| Veröffentlicht in: | Journal of Oleo Science 2020, Vol.69(12), pp.1569-1577 |
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| creator | Hara, Yasuhiro Zhang, Bo Suzuki, Akira Yamaguchi, Satoshi Adachi, Jun Tomonaga, Takeshi Yasunaga, Shin’ichiro Saku, Keijiro Aoyama, Toshiaki Hirano, Ken-ichi |
| description | Triglyceride deposit cardiomyovasculopathy (TGCV), a rare cardiovascular disorder caused by genetic or acquired dysfunction of adipose triglyceride lipase (ATGL), is marked by defective intracellular lipolysis that results in excessive accumulation of triglycerides (TGs) in the myocardium and coronary arteries, leading to intractable heart failure (HF). We have developed a specific treatment for TGCV using tricaprin, a medium chain TG, as part of a governmental rare disease project in Japan. We recently reported that tricaprin diet improved cardiac TG metabolism and left ventricular function in an ATGL-knockout (KO) mouse, a mouse model for TGCV. Here, we report the effect of tricaprin on the myocardial proteome of KO mice to elucidate the mechanisms of action of tricaprin at protein expression levels. We compared proteomic changes in the hearts of KO mice fed control or tricaprin diet. Tandem mass tag-based shotgun proteomics identified 1832 proteins common to all sample groups. Whole proteomic distribution in the heart was largely up-regulated in KO mice fed control diet. When using cut-off values (>1.5 or |
| doi_str_mv | 10.5650/jos.ess20185 |
| format | Article |
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We have developed a specific treatment for TGCV using tricaprin, a medium chain TG, as part of a governmental rare disease project in Japan. We recently reported that tricaprin diet improved cardiac TG metabolism and left ventricular function in an ATGL-knockout (KO) mouse, a mouse model for TGCV. Here, we report the effect of tricaprin on the myocardial proteome of KO mice to elucidate the mechanisms of action of tricaprin at protein expression levels. We compared proteomic changes in the hearts of KO mice fed control or tricaprin diet. Tandem mass tag-based shotgun proteomics identified 1832 proteins common to all sample groups. Whole proteomic distribution in the heart was largely up-regulated in KO mice fed control diet. When using cut-off values (>1.5 or <0.67, FDR-adjusted p value<0.01), in fact, 65 proteins were up-regulated whereas only 2 proteins were down-regulated in the hearts of KO mice fed control diet. The former included proteins assigned to “Cardiac Arrhythmia”, and “Cardiac Damage” reflecting HF by a toxicity function analysis. One of the latter was Ces1d, which is known to regulate intracellular TG metabolism. These proteomic changes observed in KO mice were dramatically rescued by the tricaprin diet. These results indicated that tricaprin diet ameliorated HF in a TGCV mouse model at protein expression levels and also provided important clues to understand mechanisms for the beneficial effect of tricaprin.</description><identifier>ISSN: 1345-8957</identifier><identifier>EISSN: 1347-3352</identifier><identifier>DOI: 10.5650/jos.ess20185</identifier><identifier>PMID: 33177279</identifier><language>eng</language><publisher>Japan: Japan Oil Chemists' Society</publisher><subject>Animals ; Arrhythmia ; Arteries ; Cardiovascular Diseases - etiology ; Cardiovascular Diseases - genetics ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - physiopathology ; Diet ; Dietary Supplements ; Disease Models, Animal ; Female ; Function analysis ; heart ; Lipase ; Lipase - physiology ; Lipolysis - drug effects ; Lipolysis - genetics ; Male ; Metabolism ; Mice, Knockout ; Myocardium ; Myocardium - metabolism ; Protein expression ; Proteins ; Proteome - metabolism ; Proteomics ; Rodents ; Shotguns ; TGCV ; Toxicity ; tricaprin ; triglyceride ; Triglycerides ; Triglycerides - administration & dosage ; Triglycerides - metabolism ; Triglycerides - pharmacology ; Ventricular Function, Left - drug effects</subject><ispartof>Journal of Oleo Science, 2020, Vol.69(12), pp.1569-1577</ispartof><rights>2020 by Japan Oil Chemists' Society</rights><rights>Copyright Japan Science and Technology Agency 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c655t-b7339bab9273ef0298d3a74af0c1efce37c4cb6f56130ea2a5258ac5d61db5af3</citedby><cites>FETCH-LOGICAL-c655t-b7339bab9273ef0298d3a74af0c1efce37c4cb6f56130ea2a5258ac5d61db5af3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33177279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hara, Yasuhiro</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Suzuki, Akira</creatorcontrib><creatorcontrib>Yamaguchi, Satoshi</creatorcontrib><creatorcontrib>Adachi, Jun</creatorcontrib><creatorcontrib>Tomonaga, Takeshi</creatorcontrib><creatorcontrib>Yasunaga, Shin’ichiro</creatorcontrib><creatorcontrib>Saku, Keijiro</creatorcontrib><creatorcontrib>Aoyama, Toshiaki</creatorcontrib><creatorcontrib>Hirano, Ken-ichi</creatorcontrib><creatorcontrib>and Nutritional Therapeutics (CNT</creatorcontrib><creatorcontrib>Non-Invasive</creatorcontrib><creatorcontrib>Novel</creatorcontrib><creatorcontrib>Laboratory of Proteome Research</creatorcontrib><creatorcontrib>Food Biotechnology Platform Promoting Project</creatorcontrib><creatorcontrib>Osaka University</creatorcontrib><creatorcontrib>Fukuoka University Medical School</creatorcontrib><creatorcontrib>National Institute of Biomedical Innovation</creatorcontrib><creatorcontrib>Graduate School of Medicine</creatorcontrib><creatorcontrib>New industry Creation Hatchery Center (NICHe at Tohoku University</creatorcontrib><creatorcontrib>Laboratory of Cardiovascular Disease</creatorcontrib><creatorcontrib>Department of Biochemistry</creatorcontrib><creatorcontrib>General Medical Research Center</creatorcontrib><creatorcontrib>Health and Nutrition</creatorcontrib><title>Effect of Tricaprin on Cardiac Proteome in a Mouse Model for Triglyceride Deposit Cardiomyovasculopathy</title><title>Journal of Oleo Science</title><addtitle>J Oleo Sci</addtitle><description>Triglyceride deposit cardiomyovasculopathy (TGCV), a rare cardiovascular disorder caused by genetic or acquired dysfunction of adipose triglyceride lipase (ATGL), is marked by defective intracellular lipolysis that results in excessive accumulation of triglycerides (TGs) in the myocardium and coronary arteries, leading to intractable heart failure (HF). We have developed a specific treatment for TGCV using tricaprin, a medium chain TG, as part of a governmental rare disease project in Japan. We recently reported that tricaprin diet improved cardiac TG metabolism and left ventricular function in an ATGL-knockout (KO) mouse, a mouse model for TGCV. Here, we report the effect of tricaprin on the myocardial proteome of KO mice to elucidate the mechanisms of action of tricaprin at protein expression levels. We compared proteomic changes in the hearts of KO mice fed control or tricaprin diet. Tandem mass tag-based shotgun proteomics identified 1832 proteins common to all sample groups. Whole proteomic distribution in the heart was largely up-regulated in KO mice fed control diet. When using cut-off values (>1.5 or <0.67, FDR-adjusted p value<0.01), in fact, 65 proteins were up-regulated whereas only 2 proteins were down-regulated in the hearts of KO mice fed control diet. The former included proteins assigned to “Cardiac Arrhythmia”, and “Cardiac Damage” reflecting HF by a toxicity function analysis. One of the latter was Ces1d, which is known to regulate intracellular TG metabolism. These proteomic changes observed in KO mice were dramatically rescued by the tricaprin diet. These results indicated that tricaprin diet ameliorated HF in a TGCV mouse model at protein expression levels and also provided important clues to understand mechanisms for the beneficial effect of tricaprin.</description><subject>Animals</subject><subject>Arrhythmia</subject><subject>Arteries</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>Diet</subject><subject>Dietary Supplements</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Function analysis</subject><subject>heart</subject><subject>Lipase</subject><subject>Lipase - physiology</subject><subject>Lipolysis - drug effects</subject><subject>Lipolysis - genetics</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice, Knockout</subject><subject>Myocardium</subject><subject>Myocardium - metabolism</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proteome - metabolism</subject><subject>Proteomics</subject><subject>Rodents</subject><subject>Shotguns</subject><subject>TGCV</subject><subject>Toxicity</subject><subject>tricaprin</subject><subject>triglyceride</subject><subject>Triglycerides</subject><subject>Triglycerides - administration & dosage</subject><subject>Triglycerides - metabolism</subject><subject>Triglycerides - pharmacology</subject><subject>Ventricular Function, Left - drug effects</subject><issn>1345-8957</issn><issn>1347-3352</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUEtP3DAQtqpW5dHeOCNLvTbUj9hOjtVCAYmqPdCzNXHGS6JsvLUTpP33eAm7XGasme8x_gi54OxKacV-9CFdYUqC8Up9IKdclqaQUomPr29VVLUyJ-QspZ6xPFfmMzmRkhsjTH1K1jfeo5to8PQxdg62sRtpGOkKYtuBo39jmDBskOYx0N9hTphriwP1Ie4p62HnMHYt0mvchtRNCzVsduEZkpuHsIXpafeFfPIwJPz61s_Jv183j6u74uHP7f3q50PhtFJT0Rgp6waaWhiJnom6aiWYEjxzHL1DaVzpGu2V5pIhCFBCVeBUq3nbKPDynHxbdLcx_J8xTbYPcxyzpRWl1szw0oiM-r6gXAwpRfQ2_3sDcWc5s_tUMyvZQ6oZfvkmOjcbbI_gQ4wZcLsA8jaHOIRx6EZ8t257EwbMkoIJZhnTNRe5KcuVrnMxRupKsVJnpdWi1KcJ1ni0gjh1bsDXu_YUsa-HA49b9wTR4ihfAA7bpBs</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Hara, Yasuhiro</creator><creator>Zhang, Bo</creator><creator>Suzuki, Akira</creator><creator>Yamaguchi, Satoshi</creator><creator>Adachi, Jun</creator><creator>Tomonaga, Takeshi</creator><creator>Yasunaga, Shin’ichiro</creator><creator>Saku, Keijiro</creator><creator>Aoyama, Toshiaki</creator><creator>Hirano, Ken-ichi</creator><general>Japan Oil Chemists' Society</general><general>Japan Science and Technology Agency</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>8FD</scope><scope>F28</scope><scope>FR3</scope></search><sort><creationdate>20200101</creationdate><title>Effect of Tricaprin on Cardiac Proteome in a Mouse Model for Triglyceride Deposit Cardiomyovasculopathy</title><author>Hara, Yasuhiro ; Zhang, Bo ; Suzuki, Akira ; Yamaguchi, Satoshi ; Adachi, Jun ; Tomonaga, Takeshi ; Yasunaga, Shin’ichiro ; Saku, Keijiro ; Aoyama, Toshiaki ; Hirano, Ken-ichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c655t-b7339bab9273ef0298d3a74af0c1efce37c4cb6f56130ea2a5258ac5d61db5af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Arrhythmia</topic><topic>Arteries</topic><topic>Cardiovascular Diseases - 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We have developed a specific treatment for TGCV using tricaprin, a medium chain TG, as part of a governmental rare disease project in Japan. We recently reported that tricaprin diet improved cardiac TG metabolism and left ventricular function in an ATGL-knockout (KO) mouse, a mouse model for TGCV. Here, we report the effect of tricaprin on the myocardial proteome of KO mice to elucidate the mechanisms of action of tricaprin at protein expression levels. We compared proteomic changes in the hearts of KO mice fed control or tricaprin diet. Tandem mass tag-based shotgun proteomics identified 1832 proteins common to all sample groups. Whole proteomic distribution in the heart was largely up-regulated in KO mice fed control diet. When using cut-off values (>1.5 or <0.67, FDR-adjusted p value<0.01), in fact, 65 proteins were up-regulated whereas only 2 proteins were down-regulated in the hearts of KO mice fed control diet. The former included proteins assigned to “Cardiac Arrhythmia”, and “Cardiac Damage” reflecting HF by a toxicity function analysis. One of the latter was Ces1d, which is known to regulate intracellular TG metabolism. These proteomic changes observed in KO mice were dramatically rescued by the tricaprin diet. These results indicated that tricaprin diet ameliorated HF in a TGCV mouse model at protein expression levels and also provided important clues to understand mechanisms for the beneficial effect of tricaprin.</abstract><cop>Japan</cop><pub>Japan Oil Chemists' Society</pub><pmid>33177279</pmid><doi>10.5650/jos.ess20185</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arrhythmia Arteries Cardiovascular Diseases - etiology Cardiovascular Diseases - genetics Cardiovascular Diseases - metabolism Cardiovascular Diseases - physiopathology Diet Dietary Supplements Disease Models, Animal Female Function analysis heart Lipase Lipase - physiology Lipolysis - drug effects Lipolysis - genetics Male Metabolism Mice, Knockout Myocardium Myocardium - metabolism Protein expression Proteins Proteome - metabolism Proteomics Rodents Shotguns TGCV Toxicity tricaprin triglyceride Triglycerides Triglycerides - administration & dosage Triglycerides - metabolism Triglycerides - pharmacology Ventricular Function, Left - drug effects |
| title | Effect of Tricaprin on Cardiac Proteome in a Mouse Model for Triglyceride Deposit Cardiomyovasculopathy |
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