Exenatide induces an increase in vasodilatory and a decrease in vasoconstrictive mediators
In view of the known vasodilatory effects of glucagon‐like peptide‐1 and exenatide, we investigated the effects of exenatide on vasoactive factors. We analysed blood samples and mononuclear cells (MNCs) from a previous study, collected after a single dose and 12 weeks of exenatide or placebo treatme...
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| Veröffentlicht in: | Diabetes, obesity & metabolism obesity & metabolism, 2017-05, Vol.19 (5), p.729-733 |
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| creator | Chaudhuri, Ajay Ghanim, Husam Makdissi, Antoine Green, Kelly Abuaysheh, Sanaa Batra, Manav D. Kuhadiya, Nitesh Dandona, Paresh |
| description | In view of the known vasodilatory effects of glucagon‐like peptide‐1 and exenatide, we investigated the effects of exenatide on vasoactive factors. We analysed blood samples and mononuclear cells (MNCs) from a previous study, collected after a single dose and 12 weeks of exenatide or placebo treatment in a series of 24 patients with type 2 diabetes mellitus. After exenatide treatment, plasma concentrations of atrial natriuretic peptide, cyclic guanyl monophosphate (cGMP) and cyclic adenyl monophosphate increased significantly at 12 weeks. Plasma cGMP and adenylate cyclase expression in MNCs increased significantly after a single dose. Angiotensinogen concentration fell significantly 2 hours after a single dose and at 12 weeks, while renin and angiotensin II levels fell significantly only after a single dose and not after 12 weeks of treatment. Exenatide also suppressed the plasma concentration of transforming growth factor‐β and the expression of P311 in MNCs at 12 weeks. Thus, exenatide induces an increase in a series of vasodilators, while suppressing the renin‐angiotensin system. These changes may contribute to the overall vasodilatory effect of exenatide. |
| doi_str_mv | 10.1111/dom.12835 |
| format | Article |
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Kuhadiya, Nitesh ; Dandona, Paresh</creator><creatorcontrib>Chaudhuri, Ajay ; Ghanim, Husam ; Makdissi, Antoine ; Green, Kelly ; Abuaysheh, Sanaa ; Batra, Manav ; D. Kuhadiya, Nitesh ; Dandona, Paresh</creatorcontrib><description>In view of the known vasodilatory effects of glucagon‐like peptide‐1 and exenatide, we investigated the effects of exenatide on vasoactive factors. We analysed blood samples and mononuclear cells (MNCs) from a previous study, collected after a single dose and 12 weeks of exenatide or placebo treatment in a series of 24 patients with type 2 diabetes mellitus. After exenatide treatment, plasma concentrations of atrial natriuretic peptide, cyclic guanyl monophosphate (cGMP) and cyclic adenyl monophosphate increased significantly at 12 weeks. Plasma cGMP and adenylate cyclase expression in MNCs increased significantly after a single dose. Angiotensinogen concentration fell significantly 2 hours after a single dose and at 12 weeks, while renin and angiotensin II levels fell significantly only after a single dose and not after 12 weeks of treatment. Exenatide also suppressed the plasma concentration of transforming growth factor‐β and the expression of P311 in MNCs at 12 weeks. Thus, exenatide induces an increase in a series of vasodilators, while suppressing the renin‐angiotensin system. These changes may contribute to the overall vasodilatory effect of exenatide.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.12835</identifier><identifier>PMID: 27891769</identifier><identifier>CODEN: DOMEF6</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenylate cyclase ; Adenylyl Cyclases - chemistry ; Adenylyl Cyclases - genetics ; Adenylyl Cyclases - metabolism ; Angiotensin ; Angiotensin II ; Angiotensinogen ; Angiotensinogen - antagonists & inhibitors ; Angiotensinogen - blood ; Anti-Obesity Agents - therapeutic use ; Antihypertensive Agents - therapeutic use ; Atrial Natriuretic Factor - agonists ; Atrial Natriuretic Factor - blood ; Atrial natriuretic peptide ; blood pressure ; Blood Pressure - drug effects ; Cyclic AMP - agonists ; Cyclic AMP - blood ; Cyclic GMP ; Cyclic GMP - agonists ; Cyclic GMP - blood ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - immunology ; Diabetes Mellitus, Type 2 - metabolism ; exenatide ; Gene Expression Regulation - drug effects ; Glucagon ; Glucagon-Like Peptide 1 - agonists ; Glucagon-Like Peptide 1 - metabolism ; Humans ; Hypoglycemic Agents - therapeutic use ; Leukocytes (mononuclear) ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - immunology ; Leukocytes, Mononuclear - metabolism ; Nerve Tissue Proteins - antagonists & inhibitors ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Obesity - blood ; Obesity - drug therapy ; Obesity - immunology ; Obesity - metabolism ; Oncogene Proteins - antagonists & inhibitors ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Peptides ; Peptides - therapeutic use ; Renin ; Renin-Angiotensin System - drug effects ; Reproducibility of Results ; Single-Blind Method ; Transforming Growth Factor beta - antagonists & inhibitors ; Transforming Growth Factor beta - blood ; Vasoactive agents ; vasodilatation ; Venoms - therapeutic use</subject><ispartof>Diabetes, obesity & metabolism, 2017-05, Vol.19 (5), p.729-733</ispartof><rights>2016 John Wiley & Sons Ltd</rights><rights>2016 John Wiley & Sons Ltd.</rights><rights>2017 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4145-b64aa335676719fa877a0e78ddacebbad2ece5981475afbf2d894737a17a476f3</citedby><cites>FETCH-LOGICAL-c4145-b64aa335676719fa877a0e78ddacebbad2ece5981475afbf2d894737a17a476f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.12835$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.12835$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27891769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chaudhuri, Ajay</creatorcontrib><creatorcontrib>Ghanim, Husam</creatorcontrib><creatorcontrib>Makdissi, Antoine</creatorcontrib><creatorcontrib>Green, Kelly</creatorcontrib><creatorcontrib>Abuaysheh, Sanaa</creatorcontrib><creatorcontrib>Batra, Manav</creatorcontrib><creatorcontrib>D. Kuhadiya, Nitesh</creatorcontrib><creatorcontrib>Dandona, Paresh</creatorcontrib><title>Exenatide induces an increase in vasodilatory and a decrease in vasoconstrictive mediators</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>In view of the known vasodilatory effects of glucagon‐like peptide‐1 and exenatide, we investigated the effects of exenatide on vasoactive factors. We analysed blood samples and mononuclear cells (MNCs) from a previous study, collected after a single dose and 12 weeks of exenatide or placebo treatment in a series of 24 patients with type 2 diabetes mellitus. After exenatide treatment, plasma concentrations of atrial natriuretic peptide, cyclic guanyl monophosphate (cGMP) and cyclic adenyl monophosphate increased significantly at 12 weeks. Plasma cGMP and adenylate cyclase expression in MNCs increased significantly after a single dose. Angiotensinogen concentration fell significantly 2 hours after a single dose and at 12 weeks, while renin and angiotensin II levels fell significantly only after a single dose and not after 12 weeks of treatment. Exenatide also suppressed the plasma concentration of transforming growth factor‐β and the expression of P311 in MNCs at 12 weeks. Thus, exenatide induces an increase in a series of vasodilators, while suppressing the renin‐angiotensin system. These changes may contribute to the overall vasodilatory effect of exenatide.</description><subject>Adenylate cyclase</subject><subject>Adenylyl Cyclases - chemistry</subject><subject>Adenylyl Cyclases - genetics</subject><subject>Adenylyl Cyclases - metabolism</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensinogen</subject><subject>Angiotensinogen - antagonists & inhibitors</subject><subject>Angiotensinogen - blood</subject><subject>Anti-Obesity Agents - therapeutic use</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>Atrial Natriuretic Factor - agonists</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Atrial natriuretic peptide</subject><subject>blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Cyclic AMP - agonists</subject><subject>Cyclic AMP - blood</subject><subject>Cyclic GMP</subject><subject>Cyclic GMP - agonists</subject><subject>Cyclic GMP - blood</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>exenatide</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucagon</subject><subject>Glucagon-Like Peptide 1 - agonists</subject><subject>Glucagon-Like Peptide 1 - metabolism</subject><subject>Humans</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Leukocytes (mononuclear)</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Nerve Tissue Proteins - antagonists & inhibitors</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Obesity - blood</subject><subject>Obesity - drug therapy</subject><subject>Obesity - immunology</subject><subject>Obesity - metabolism</subject><subject>Oncogene Proteins - antagonists & inhibitors</subject><subject>Oncogene Proteins - genetics</subject><subject>Oncogene Proteins - metabolism</subject><subject>Peptides</subject><subject>Peptides - therapeutic use</subject><subject>Renin</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Reproducibility of Results</subject><subject>Single-Blind Method</subject><subject>Transforming Growth Factor beta - antagonists & inhibitors</subject><subject>Transforming Growth Factor beta - blood</subject><subject>Vasoactive agents</subject><subject>vasodilatation</subject><subject>Venoms - therapeutic use</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1L5jAQx8Oy4tvuwS8ghb3ooZq3Nslx8R0UL3rZS5gmU4j0ad2kVZ9vb-rjCi6ogSFD5sd_MvMnZIfRA5bPoR8WB4xrUX0jm0zWomSC199fcl5qQ_kG2UrpjlIqhVbrZIMrbZiqzSb5c_KEPYzBYxF6PzlMBfQ5dREhzW_FA6TBhw7GIS5zzRdQeHxfdkOfxhjcGB6wWKAPM5x-kLUWuoQ_X-9tcnt6cnN0Xl5en10c_b4snWSyKptaAghR1apWzLSglQKKSnsPDpsGPEeHldFMqgrapuVeG6mEAqZAqroV22RvpXsfh78TptEuQnLYddDjMCXL8qxaizm-RqXMP6lqltFf_6F3wxT7PIgVtDKSc270Z1TuZzjlQszU_opycUgpYmvvY1hAXFpG7eygzQ7aFwczu_uqODV5lW_kP8sycLgCHkOHy4-V7PH11UryGc95pBo</recordid><startdate>201705</startdate><enddate>201705</enddate><creator>Chaudhuri, Ajay</creator><creator>Ghanim, Husam</creator><creator>Makdissi, Antoine</creator><creator>Green, Kelly</creator><creator>Abuaysheh, Sanaa</creator><creator>Batra, Manav</creator><creator>D. Kuhadiya, Nitesh</creator><creator>Dandona, Paresh</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201705</creationdate><title>Exenatide induces an increase in vasodilatory and a decrease in vasoconstrictive mediators</title><author>Chaudhuri, Ajay ; Ghanim, Husam ; Makdissi, Antoine ; Green, Kelly ; Abuaysheh, Sanaa ; Batra, Manav ; D. Kuhadiya, Nitesh ; Dandona, Paresh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4145-b64aa335676719fa877a0e78ddacebbad2ece5981475afbf2d894737a17a476f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenylate cyclase</topic><topic>Adenylyl Cyclases - chemistry</topic><topic>Adenylyl Cyclases - genetics</topic><topic>Adenylyl Cyclases - metabolism</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensinogen</topic><topic>Angiotensinogen - antagonists & inhibitors</topic><topic>Angiotensinogen - blood</topic><topic>Anti-Obesity Agents - therapeutic use</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>Atrial Natriuretic Factor - agonists</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Atrial natriuretic peptide</topic><topic>blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Cyclic AMP - agonists</topic><topic>Cyclic AMP - blood</topic><topic>Cyclic GMP</topic><topic>Cyclic GMP - agonists</topic><topic>Cyclic GMP - blood</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>exenatide</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glucagon</topic><topic>Glucagon-Like Peptide 1 - agonists</topic><topic>Glucagon-Like Peptide 1 - metabolism</topic><topic>Humans</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Leukocytes (mononuclear)</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Nerve Tissue Proteins - antagonists & inhibitors</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Obesity - blood</topic><topic>Obesity - drug therapy</topic><topic>Obesity - immunology</topic><topic>Obesity - metabolism</topic><topic>Oncogene Proteins - antagonists & inhibitors</topic><topic>Oncogene Proteins - genetics</topic><topic>Oncogene Proteins - metabolism</topic><topic>Peptides</topic><topic>Peptides - therapeutic use</topic><topic>Renin</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Reproducibility of Results</topic><topic>Single-Blind Method</topic><topic>Transforming Growth Factor beta - antagonists & inhibitors</topic><topic>Transforming Growth Factor beta - blood</topic><topic>Vasoactive agents</topic><topic>vasodilatation</topic><topic>Venoms - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chaudhuri, Ajay</creatorcontrib><creatorcontrib>Ghanim, Husam</creatorcontrib><creatorcontrib>Makdissi, Antoine</creatorcontrib><creatorcontrib>Green, Kelly</creatorcontrib><creatorcontrib>Abuaysheh, Sanaa</creatorcontrib><creatorcontrib>Batra, Manav</creatorcontrib><creatorcontrib>D. Kuhadiya, Nitesh</creatorcontrib><creatorcontrib>Dandona, Paresh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chaudhuri, Ajay</au><au>Ghanim, Husam</au><au>Makdissi, Antoine</au><au>Green, Kelly</au><au>Abuaysheh, Sanaa</au><au>Batra, Manav</au><au>D. Kuhadiya, Nitesh</au><au>Dandona, Paresh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exenatide induces an increase in vasodilatory and a decrease in vasoconstrictive mediators</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2017-05</date><risdate>2017</risdate><volume>19</volume><issue>5</issue><spage>729</spage><epage>733</epage><pages>729-733</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><coden>DOMEF6</coden><abstract>In view of the known vasodilatory effects of glucagon‐like peptide‐1 and exenatide, we investigated the effects of exenatide on vasoactive factors. We analysed blood samples and mononuclear cells (MNCs) from a previous study, collected after a single dose and 12 weeks of exenatide or placebo treatment in a series of 24 patients with type 2 diabetes mellitus. After exenatide treatment, plasma concentrations of atrial natriuretic peptide, cyclic guanyl monophosphate (cGMP) and cyclic adenyl monophosphate increased significantly at 12 weeks. Plasma cGMP and adenylate cyclase expression in MNCs increased significantly after a single dose. Angiotensinogen concentration fell significantly 2 hours after a single dose and at 12 weeks, while renin and angiotensin II levels fell significantly only after a single dose and not after 12 weeks of treatment. Exenatide also suppressed the plasma concentration of transforming growth factor‐β and the expression of P311 in MNCs at 12 weeks. Thus, exenatide induces an increase in a series of vasodilators, while suppressing the renin‐angiotensin system. These changes may contribute to the overall vasodilatory effect of exenatide.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>27891769</pmid><doi>10.1111/dom.12835</doi><tpages>5</tpages></addata></record> |
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| ispartof | Diabetes, obesity & metabolism, 2017-05, Vol.19 (5), p.729-733 |
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| subjects | Adenylate cyclase Adenylyl Cyclases - chemistry Adenylyl Cyclases - genetics Adenylyl Cyclases - metabolism Angiotensin Angiotensin II Angiotensinogen Angiotensinogen - antagonists & inhibitors Angiotensinogen - blood Anti-Obesity Agents - therapeutic use Antihypertensive Agents - therapeutic use Atrial Natriuretic Factor - agonists Atrial Natriuretic Factor - blood Atrial natriuretic peptide blood pressure Blood Pressure - drug effects Cyclic AMP - agonists Cyclic AMP - blood Cyclic GMP Cyclic GMP - agonists Cyclic GMP - blood Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - immunology Diabetes Mellitus, Type 2 - metabolism exenatide Gene Expression Regulation - drug effects Glucagon Glucagon-Like Peptide 1 - agonists Glucagon-Like Peptide 1 - metabolism Humans Hypoglycemic Agents - therapeutic use Leukocytes (mononuclear) Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Nerve Tissue Proteins - antagonists & inhibitors Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Obesity - blood Obesity - drug therapy Obesity - immunology Obesity - metabolism Oncogene Proteins - antagonists & inhibitors Oncogene Proteins - genetics Oncogene Proteins - metabolism Peptides Peptides - therapeutic use Renin Renin-Angiotensin System - drug effects Reproducibility of Results Single-Blind Method Transforming Growth Factor beta - antagonists & inhibitors Transforming Growth Factor beta - blood Vasoactive agents vasodilatation Venoms - therapeutic use |
| title | Exenatide induces an increase in vasodilatory and a decrease in vasoconstrictive mediators |
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