Increased tissue kallikrein levels in type 2 diabetes
Aims/hypothesis We measured components of the kallikrein-kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. Methods Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well...
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| Veröffentlicht in: | Diabetologia 2010-04, Vol.53 (4), p.779-785 |
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| creator | Campbell, D. J Kladis, A Zhang, Y Jenkins, A. J Prior, D. L Yii, M Kenny, J. F Black, M. J Kelly, D. J |
| description | Aims/hypothesis We measured components of the kallikrein-kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. Methods Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well as plasma and tissue kallikrein, and kallistatin were measured in non-diabetic and diabetic patients before coronary artery bypass graft surgery. Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantified. Results Plasma levels of tissue kallikrein were approximately 62% higher in diabetic than in non-diabetic patients (p = 0.001), whereas no differences were seen in circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, or in plasma kallikrein or kallistatin. Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes (p = 0.015), while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients (p = 0.014). Statin therapy did not change any variables of the circulating kallikrein-kinin system. Neither aspirin, calcium antagonists, beta blockers or long-acting nitrate therapies influenced any kallikrein-kinin system variable. Conclusions/interpretation Tissue kallikrein levels are increased in type 2 diabetes, whereas statin therapy does not modify the circulating kallikrein-kinin system. Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in non-diabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients. However, our findings do not support a role for the kallikrein-kinin system in mediating the effects of statin therapy on endothelial function. |
| doi_str_mv | 10.1007/s00125-009-1645-8 |
| format | Article |
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J ; Kladis, A ; Zhang, Y ; Jenkins, A. J ; Prior, D. L ; Yii, M ; Kenny, J. F ; Black, M. J ; Kelly, D. J</creator><creatorcontrib>Campbell, D. J ; Kladis, A ; Zhang, Y ; Jenkins, A. J ; Prior, D. L ; Yii, M ; Kenny, J. F ; Black, M. J ; Kelly, D. J</creatorcontrib><description>Aims/hypothesis We measured components of the kallikrein-kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. Methods Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well as plasma and tissue kallikrein, and kallistatin were measured in non-diabetic and diabetic patients before coronary artery bypass graft surgery. Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantified. Results Plasma levels of tissue kallikrein were approximately 62% higher in diabetic than in non-diabetic patients (p = 0.001), whereas no differences were seen in circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, or in plasma kallikrein or kallistatin. Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes (p = 0.015), while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients (p = 0.014). Statin therapy did not change any variables of the circulating kallikrein-kinin system. Neither aspirin, calcium antagonists, beta blockers or long-acting nitrate therapies influenced any kallikrein-kinin system variable. Conclusions/interpretation Tissue kallikrein levels are increased in type 2 diabetes, whereas statin therapy does not modify the circulating kallikrein-kinin system. Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in non-diabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients. However, our findings do not support a role for the kallikrein-kinin system in mediating the effects of statin therapy on endothelial function.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-009-1645-8</identifier><identifier>PMID: 20225398</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Aspirin ; Biological and medical sciences ; Cardiotonic Agents - blood ; Cardiovascular disease ; Coronary Artery Bypass ; Coronary vessels ; Diabetes ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - enzymology ; Diabetes. Impaired glucose tolerance ; Diabetic Angiopathies - blood ; Diabetic Angiopathies - drug therapy ; Diabetic Angiopathies - surgery ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiopathology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Heart surgery ; Human Physiology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Hypotheses ; Immunohistochemistry ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Molecular weight ; Patients ; Peptides ; RNA, Messenger - genetics ; Tissue Kallikreins - blood ; Tissue Kallikreins - genetics ; Vein & artery diseases</subject><ispartof>Diabetologia, 2010-04, Vol.53 (4), p.779-785</ispartof><rights>Springer-Verlag 2009</rights><rights>2015 INIST-CNRS</rights><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-219ee81265419d692ce60fb43199901553891ba70cb7d2ff8dfa2329d9668e3e3</citedby><cites>FETCH-LOGICAL-c467t-219ee81265419d692ce60fb43199901553891ba70cb7d2ff8dfa2329d9668e3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-009-1645-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-009-1645-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22536611$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20225398$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Campbell, D. J</creatorcontrib><creatorcontrib>Kladis, A</creatorcontrib><creatorcontrib>Zhang, Y</creatorcontrib><creatorcontrib>Jenkins, A. J</creatorcontrib><creatorcontrib>Prior, D. L</creatorcontrib><creatorcontrib>Yii, M</creatorcontrib><creatorcontrib>Kenny, J. F</creatorcontrib><creatorcontrib>Black, M. J</creatorcontrib><creatorcontrib>Kelly, D. J</creatorcontrib><title>Increased tissue kallikrein levels in type 2 diabetes</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis We measured components of the kallikrein-kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. Methods Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well as plasma and tissue kallikrein, and kallistatin were measured in non-diabetic and diabetic patients before coronary artery bypass graft surgery. Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantified. Results Plasma levels of tissue kallikrein were approximately 62% higher in diabetic than in non-diabetic patients (p = 0.001), whereas no differences were seen in circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, or in plasma kallikrein or kallistatin. Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes (p = 0.015), while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients (p = 0.014). Statin therapy did not change any variables of the circulating kallikrein-kinin system. Neither aspirin, calcium antagonists, beta blockers or long-acting nitrate therapies influenced any kallikrein-kinin system variable. Conclusions/interpretation Tissue kallikrein levels are increased in type 2 diabetes, whereas statin therapy does not modify the circulating kallikrein-kinin system. Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in non-diabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients. However, our findings do not support a role for the kallikrein-kinin system in mediating the effects of statin therapy on endothelial function.</description><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Aspirin</subject><subject>Biological and medical sciences</subject><subject>Cardiotonic Agents - blood</subject><subject>Cardiovascular disease</subject><subject>Coronary Artery Bypass</subject><subject>Coronary vessels</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - enzymology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Angiopathies - blood</subject><subject>Diabetic Angiopathies - drug therapy</subject><subject>Diabetic Angiopathies - surgery</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Heart surgery</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Hypotheses</subject><subject>Immunohistochemistry</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Molecular weight</subject><subject>Patients</subject><subject>Peptides</subject><subject>RNA, Messenger - genetics</subject><subject>Tissue Kallikreins - blood</subject><subject>Tissue Kallikreins - genetics</subject><subject>Vein & artery diseases</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kEtr3EAQhIeQEK-d_IBcEhEwOcnpnpdmjsbkYTDk4BhyG0ZSy8jWSptpKeB_71m0iSEHn7qhv6ouSoh3CGcIUH1mAJSmBPAlWm1K90JsUCtZgpbupdjszyU6--tIHDPfAYAy2r4WRxKkNMq7jTCXY5MoMrXF3DMvVNzHYejvE_VjMdAfGrjI2_ywo0IWbR9rmonfiFddHJjeHuaJuPn65efF9_Lqx7fLi_OrstG2mkuJnsihtEajb62XDVnoaq3Qew9ojHIe61hBU1et7DrXdlEq6VtvrSNF6kR8Wn13afq9EM9h23NDwxBHmhYOlVJV9rGYyY__kXfTksYcLkhUTmuNkCFcoSZNzIm6sEv9NqaHgBD2jYa10ZAbDftGg8ua9wfjpd5S-0_xt8IMnB6AyE0cuhTHpucnLlPW4j6hXDnOp_GW0lPC575_WEVdnEK8Tdn45loCKkCHCEarR_C0k-A</recordid><startdate>20100401</startdate><enddate>20100401</enddate><creator>Campbell, D. 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Impaired glucose tolerance</topic><topic>Diabetic Angiopathies - blood</topic><topic>Diabetic Angiopathies - drug therapy</topic><topic>Diabetic Angiopathies - surgery</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Heart surgery</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Hypotheses</topic><topic>Immunohistochemistry</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Molecular weight</topic><topic>Patients</topic><topic>Peptides</topic><topic>RNA, Messenger - genetics</topic><topic>Tissue Kallikreins - blood</topic><topic>Tissue Kallikreins - genetics</topic><topic>Vein & artery diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Campbell, D. J</creatorcontrib><creatorcontrib>Kladis, A</creatorcontrib><creatorcontrib>Zhang, Y</creatorcontrib><creatorcontrib>Jenkins, A. J</creatorcontrib><creatorcontrib>Prior, D. 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J</creatorcontrib><collection>AGRIS</collection><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>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Campbell, D. J</au><au>Kladis, A</au><au>Zhang, Y</au><au>Jenkins, A. J</au><au>Prior, D. L</au><au>Yii, M</au><au>Kenny, J. F</au><au>Black, M. J</au><au>Kelly, D. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased tissue kallikrein levels in type 2 diabetes</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2010-04-01</date><risdate>2010</risdate><volume>53</volume><issue>4</issue><spage>779</spage><epage>785</epage><pages>779-785</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis We measured components of the kallikrein-kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. Methods Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well as plasma and tissue kallikrein, and kallistatin were measured in non-diabetic and diabetic patients before coronary artery bypass graft surgery. Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantified. Results Plasma levels of tissue kallikrein were approximately 62% higher in diabetic than in non-diabetic patients (p = 0.001), whereas no differences were seen in circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, or in plasma kallikrein or kallistatin. Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes (p = 0.015), while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients (p = 0.014). Statin therapy did not change any variables of the circulating kallikrein-kinin system. Neither aspirin, calcium antagonists, beta blockers or long-acting nitrate therapies influenced any kallikrein-kinin system variable. Conclusions/interpretation Tissue kallikrein levels are increased in type 2 diabetes, whereas statin therapy does not modify the circulating kallikrein-kinin system. Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in non-diabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients. However, our findings do not support a role for the kallikrein-kinin system in mediating the effects of statin therapy on endothelial function.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>20225398</pmid><doi>10.1007/s00125-009-1645-8</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin-Converting Enzyme Inhibitors - therapeutic use Aspirin Biological and medical sciences Cardiotonic Agents - blood Cardiovascular disease Coronary Artery Bypass Coronary vessels Diabetes Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - enzymology Diabetes. Impaired glucose tolerance Diabetic Angiopathies - blood Diabetic Angiopathies - drug therapy Diabetic Angiopathies - surgery Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endothelium, Vascular - drug effects Endothelium, Vascular - physiopathology Etiopathogenesis. Screening. Investigations. Target tissue resistance Heart surgery Human Physiology Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Hypotheses Immunohistochemistry Internal Medicine Medical sciences Medicine Medicine & Public Health Metabolic Diseases Molecular weight Patients Peptides RNA, Messenger - genetics Tissue Kallikreins - blood Tissue Kallikreins - genetics Vein & artery diseases |
| title | Increased tissue kallikrein levels in type 2 diabetes |
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