Pioglitazone attenuates cardiac hypertrophy in rats with salt-sensitive hypertension: role of activation of AMP-activated protein kinase and inhibition of Akt
OBJECTIVECardiac hypertrophy is common in diabetes and an independent risk factor for cardiac morbidity and mortality. We investigated the effects of pioglitazone on cardiac hypertrophy and hypertrophic signaling in Dahl salt-sensitive hypertensive rats. METHODSDahl salt-sensitive rats were fed a hi...
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| Veröffentlicht in: | Journal of hypertension 2008-08, Vol.26 (8), p.1669-1676 |
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| creator | Kato, Mayuko F Shibata, Rei Obata, Koji Miyachi, Masaaki Yazawa, Hiroki Tsuboi, Koji Yamada, Takashi Nishizawa, Takao Noda, Akiko Cheng, Xian Wu Murate, Takashi Koike, Yasuo Murohara, Toyoaki Yokota, Mitsuhiro Nagata, Kohzo |
| description | OBJECTIVECardiac hypertrophy is common in diabetes and an independent risk factor for cardiac morbidity and mortality. We investigated the effects of pioglitazone on cardiac hypertrophy and hypertrophic signaling in Dahl salt-sensitive hypertensive rats.
METHODSDahl salt-sensitive rats were fed a high-salt diet from 7 weeks of age and treated with pioglitazone (2.5 mg/kg per day) or vehicle from 7 to 11 weeks.
RESULTSThe vehicle-treated rats developed left ventricular hypertrophy and fibrosis as well as left ventricular diastolic dysfunction. The serum level of adiponectin and the phosphorylation of AMP-activated protein kinase in the myocardium did not differ between the vehicle-treated rats and control rats maintained on a normal diet. The phosphorylation of Akt, mammalian target of rapamycin, and p70S6 kinase as well as the total protein content were increased in the heart of vehicle-treated rats compared with control rats, and these changes were blocked by treatment with pioglitazone. Pioglitazone treatment also ameliorated left ventricular hypertrophy and fibrosis, improved diastolic function, and increased both the serum adiponectin concentration and the level of AMP-activated protein kinase phosphorylation in the heart.
CONCLUSIONSLong-term administration of pioglitazone attenuated left ventricular hypertrophy and fibrosis as well as inhibited phosphorylation of mammalian target of rapamycin and p70S6 kinase in the heart of hypertensive rats. The beneficial cardiac effects of pioglitazone are likely attributable, at least partly, both to the activation of AMP-activated protein kinase signaling through stimulation of adiponectin secretion and to the inhibition of Akt signaling. |
| doi_str_mv | 10.1097/HJH.0b013e328302f0f7 |
| format | Article |
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METHODSDahl salt-sensitive rats were fed a high-salt diet from 7 weeks of age and treated with pioglitazone (2.5 mg/kg per day) or vehicle from 7 to 11 weeks.
RESULTSThe vehicle-treated rats developed left ventricular hypertrophy and fibrosis as well as left ventricular diastolic dysfunction. The serum level of adiponectin and the phosphorylation of AMP-activated protein kinase in the myocardium did not differ between the vehicle-treated rats and control rats maintained on a normal diet. The phosphorylation of Akt, mammalian target of rapamycin, and p70S6 kinase as well as the total protein content were increased in the heart of vehicle-treated rats compared with control rats, and these changes were blocked by treatment with pioglitazone. Pioglitazone treatment also ameliorated left ventricular hypertrophy and fibrosis, improved diastolic function, and increased both the serum adiponectin concentration and the level of AMP-activated protein kinase phosphorylation in the heart.
CONCLUSIONSLong-term administration of pioglitazone attenuated left ventricular hypertrophy and fibrosis as well as inhibited phosphorylation of mammalian target of rapamycin and p70S6 kinase in the heart of hypertensive rats. The beneficial cardiac effects of pioglitazone are likely attributable, at least partly, both to the activation of AMP-activated protein kinase signaling through stimulation of adiponectin secretion and to the inhibition of Akt signaling.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0b013e328302f0f7</identifier><identifier>PMID: 18622247</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Adiponectin - blood ; AMP-Activated Protein Kinases ; Animals ; Arterial hypertension. Arterial hypotension ; Atrial Natriuretic Factor - genetics ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Collagen - genetics ; Echocardiography ; Experimental diseases ; Fibrosis ; Hypertension - drug therapy ; Hypertension - metabolism ; Hypertrophy, Left Ventricular - diagnostic imaging ; Hypertrophy, Left Ventricular - drug therapy ; Hypertrophy, Left Ventricular - metabolism ; Hypoglycemic Agents - pharmacology ; Male ; Medical sciences ; Multienzyme Complexes - metabolism ; Myocardium - pathology ; Myocytes, Cardiac - pathology ; Natriuretic Peptide, Brain - genetics ; Phosphorylation - drug effects ; Protein-Serine-Threonine Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Inbred Dahl ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Thiazolidinediones - pharmacology ; Transcription Factors - metabolism</subject><ispartof>Journal of hypertension, 2008-08, Vol.26 (8), p.1669-1676</ispartof><rights>2008 Lippincott Williams & Wilkins, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3805-e357625136015e468d1ce908643f018ecf724e68dd78fa407e377b45a11fbd2a3</citedby><cites>FETCH-LOGICAL-c3805-e357625136015e468d1ce908643f018ecf724e68dd78fa407e377b45a11fbd2a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20492468$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18622247$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kato, Mayuko F</creatorcontrib><creatorcontrib>Shibata, Rei</creatorcontrib><creatorcontrib>Obata, Koji</creatorcontrib><creatorcontrib>Miyachi, Masaaki</creatorcontrib><creatorcontrib>Yazawa, Hiroki</creatorcontrib><creatorcontrib>Tsuboi, Koji</creatorcontrib><creatorcontrib>Yamada, Takashi</creatorcontrib><creatorcontrib>Nishizawa, Takao</creatorcontrib><creatorcontrib>Noda, Akiko</creatorcontrib><creatorcontrib>Cheng, Xian Wu</creatorcontrib><creatorcontrib>Murate, Takashi</creatorcontrib><creatorcontrib>Koike, Yasuo</creatorcontrib><creatorcontrib>Murohara, Toyoaki</creatorcontrib><creatorcontrib>Yokota, Mitsuhiro</creatorcontrib><creatorcontrib>Nagata, Kohzo</creatorcontrib><title>Pioglitazone attenuates cardiac hypertrophy in rats with salt-sensitive hypertension: role of activation of AMP-activated protein kinase and inhibition of Akt</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>OBJECTIVECardiac hypertrophy is common in diabetes and an independent risk factor for cardiac morbidity and mortality. We investigated the effects of pioglitazone on cardiac hypertrophy and hypertrophic signaling in Dahl salt-sensitive hypertensive rats.
METHODSDahl salt-sensitive rats were fed a high-salt diet from 7 weeks of age and treated with pioglitazone (2.5 mg/kg per day) or vehicle from 7 to 11 weeks.
RESULTSThe vehicle-treated rats developed left ventricular hypertrophy and fibrosis as well as left ventricular diastolic dysfunction. The serum level of adiponectin and the phosphorylation of AMP-activated protein kinase in the myocardium did not differ between the vehicle-treated rats and control rats maintained on a normal diet. The phosphorylation of Akt, mammalian target of rapamycin, and p70S6 kinase as well as the total protein content were increased in the heart of vehicle-treated rats compared with control rats, and these changes were blocked by treatment with pioglitazone. Pioglitazone treatment also ameliorated left ventricular hypertrophy and fibrosis, improved diastolic function, and increased both the serum adiponectin concentration and the level of AMP-activated protein kinase phosphorylation in the heart.
CONCLUSIONSLong-term administration of pioglitazone attenuated left ventricular hypertrophy and fibrosis as well as inhibited phosphorylation of mammalian target of rapamycin and p70S6 kinase in the heart of hypertensive rats. The beneficial cardiac effects of pioglitazone are likely attributable, at least partly, both to the activation of AMP-activated protein kinase signaling through stimulation of adiponectin secretion and to the inhibition of Akt signaling.</description><subject>Adiponectin - blood</subject><subject>AMP-Activated Protein Kinases</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Atrial Natriuretic Factor - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Collagen - genetics</subject><subject>Echocardiography</subject><subject>Experimental diseases</subject><subject>Fibrosis</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - metabolism</subject><subject>Hypertrophy, Left Ventricular - diagnostic imaging</subject><subject>Hypertrophy, Left Ventricular - drug therapy</subject><subject>Hypertrophy, Left Ventricular - metabolism</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Natriuretic Peptide, Brain - genetics</subject><subject>Phosphorylation - drug effects</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Transcription Factors - metabolism</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1u1DAQgC0EokvhDRDyBW4p47_Y4VZV0AUV0QOcI28yJmaz8WI7rJaH6bPiVaNWQpZlzfibGVsfIa8ZXDBo9Pv1l_UFbIAJFNwI4A6cfkJWTGpRKdWYp2QFvBZVLRQ_Iy9S-gUAptHiOTljpuacS70id7c-_Bx9tn_DhNTmjNNsMyba2dh729HhuMeYY9gPR-onGm1O9ODzQJMdc5VwSj77P7hwpzBMH2gMI9LgqO3Kpc0ld4ouv95WSwZ7uo8hY2m59ZNNZfbUlwGD3_gHfJtfkmfOjglfLec5-fHp4_erdXXz7frz1eVN1QkDqkKhdM0VEzUwhbI2PeuwAVNL4YAZ7JzmEku618ZZCRqF1hupLGNu03Mrzsm7-77lUb9nTLnd-dThONoJw5zauhG8VqIpoLwHuxhSiujaffQ7G48tg_bkpS1e2v-9lLI3S_95s8P-sWgRUYC3C2BTZ0cX7dT59MBxkA0v_3qcfwhjxpi243zA2A5YbAxtMQzSaF7xorosgKpsrsQ_ssmp1g</recordid><startdate>200808</startdate><enddate>200808</enddate><creator>Kato, Mayuko F</creator><creator>Shibata, Rei</creator><creator>Obata, Koji</creator><creator>Miyachi, Masaaki</creator><creator>Yazawa, Hiroki</creator><creator>Tsuboi, Koji</creator><creator>Yamada, Takashi</creator><creator>Nishizawa, Takao</creator><creator>Noda, Akiko</creator><creator>Cheng, Xian Wu</creator><creator>Murate, Takashi</creator><creator>Koike, Yasuo</creator><creator>Murohara, Toyoaki</creator><creator>Yokota, Mitsuhiro</creator><creator>Nagata, Kohzo</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><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>200808</creationdate><title>Pioglitazone attenuates cardiac hypertrophy in rats with salt-sensitive hypertension: role of activation of AMP-activated protein kinase and inhibition of Akt</title><author>Kato, Mayuko F ; Shibata, Rei ; Obata, Koji ; Miyachi, Masaaki ; Yazawa, Hiroki ; Tsuboi, Koji ; Yamada, Takashi ; Nishizawa, Takao ; Noda, Akiko ; Cheng, Xian Wu ; Murate, Takashi ; Koike, Yasuo ; Murohara, Toyoaki ; Yokota, Mitsuhiro ; Nagata, Kohzo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3805-e357625136015e468d1ce908643f018ecf724e68dd78fa407e377b45a11fbd2a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adiponectin - blood</topic><topic>AMP-Activated Protein Kinases</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Atrial Natriuretic Factor - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Collagen - genetics</topic><topic>Echocardiography</topic><topic>Experimental diseases</topic><topic>Fibrosis</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - metabolism</topic><topic>Hypertrophy, Left Ventricular - diagnostic imaging</topic><topic>Hypertrophy, Left Ventricular - drug therapy</topic><topic>Hypertrophy, Left Ventricular - metabolism</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Multienzyme Complexes - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Natriuretic Peptide, Brain - genetics</topic><topic>Phosphorylation - drug effects</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kato, Mayuko F</creatorcontrib><creatorcontrib>Shibata, Rei</creatorcontrib><creatorcontrib>Obata, Koji</creatorcontrib><creatorcontrib>Miyachi, Masaaki</creatorcontrib><creatorcontrib>Yazawa, Hiroki</creatorcontrib><creatorcontrib>Tsuboi, Koji</creatorcontrib><creatorcontrib>Yamada, Takashi</creatorcontrib><creatorcontrib>Nishizawa, Takao</creatorcontrib><creatorcontrib>Noda, Akiko</creatorcontrib><creatorcontrib>Cheng, Xian Wu</creatorcontrib><creatorcontrib>Murate, Takashi</creatorcontrib><creatorcontrib>Koike, Yasuo</creatorcontrib><creatorcontrib>Murohara, Toyoaki</creatorcontrib><creatorcontrib>Yokota, Mitsuhiro</creatorcontrib><creatorcontrib>Nagata, Kohzo</creatorcontrib><collection>Pascal-Francis</collection><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>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kato, Mayuko F</au><au>Shibata, Rei</au><au>Obata, Koji</au><au>Miyachi, Masaaki</au><au>Yazawa, Hiroki</au><au>Tsuboi, Koji</au><au>Yamada, Takashi</au><au>Nishizawa, Takao</au><au>Noda, Akiko</au><au>Cheng, Xian Wu</au><au>Murate, Takashi</au><au>Koike, Yasuo</au><au>Murohara, Toyoaki</au><au>Yokota, Mitsuhiro</au><au>Nagata, Kohzo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pioglitazone attenuates cardiac hypertrophy in rats with salt-sensitive hypertension: role of activation of AMP-activated protein kinase and inhibition of Akt</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2008-08</date><risdate>2008</risdate><volume>26</volume><issue>8</issue><spage>1669</spage><epage>1676</epage><pages>1669-1676</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract>OBJECTIVECardiac hypertrophy is common in diabetes and an independent risk factor for cardiac morbidity and mortality. We investigated the effects of pioglitazone on cardiac hypertrophy and hypertrophic signaling in Dahl salt-sensitive hypertensive rats.
METHODSDahl salt-sensitive rats were fed a high-salt diet from 7 weeks of age and treated with pioglitazone (2.5 mg/kg per day) or vehicle from 7 to 11 weeks.
RESULTSThe vehicle-treated rats developed left ventricular hypertrophy and fibrosis as well as left ventricular diastolic dysfunction. The serum level of adiponectin and the phosphorylation of AMP-activated protein kinase in the myocardium did not differ between the vehicle-treated rats and control rats maintained on a normal diet. The phosphorylation of Akt, mammalian target of rapamycin, and p70S6 kinase as well as the total protein content were increased in the heart of vehicle-treated rats compared with control rats, and these changes were blocked by treatment with pioglitazone. Pioglitazone treatment also ameliorated left ventricular hypertrophy and fibrosis, improved diastolic function, and increased both the serum adiponectin concentration and the level of AMP-activated protein kinase phosphorylation in the heart.
CONCLUSIONSLong-term administration of pioglitazone attenuated left ventricular hypertrophy and fibrosis as well as inhibited phosphorylation of mammalian target of rapamycin and p70S6 kinase in the heart of hypertensive rats. The beneficial cardiac effects of pioglitazone are likely attributable, at least partly, both to the activation of AMP-activated protein kinase signaling through stimulation of adiponectin secretion and to the inhibition of Akt signaling.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>18622247</pmid><doi>10.1097/HJH.0b013e328302f0f7</doi><tpages>8</tpages></addata></record> |
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| subjects | Adiponectin - blood AMP-Activated Protein Kinases Animals Arterial hypertension. Arterial hypotension Atrial Natriuretic Factor - genetics Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Collagen - genetics Echocardiography Experimental diseases Fibrosis Hypertension - drug therapy Hypertension - metabolism Hypertrophy, Left Ventricular - diagnostic imaging Hypertrophy, Left Ventricular - drug therapy Hypertrophy, Left Ventricular - metabolism Hypoglycemic Agents - pharmacology Male Medical sciences Multienzyme Complexes - metabolism Myocardium - pathology Myocytes, Cardiac - pathology Natriuretic Peptide, Brain - genetics Phosphorylation - drug effects Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Inbred Dahl Ribosomal Protein S6 Kinases, 70-kDa - metabolism RNA, Messenger - metabolism Signal Transduction - drug effects Thiazolidinediones - pharmacology Transcription Factors - metabolism |
| title | Pioglitazone attenuates cardiac hypertrophy in rats with salt-sensitive hypertension: role of activation of AMP-activated protein kinase and inhibition of Akt |
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