528-P: The Effect of Angiotensin II (ANG II) Infusion on Plasma Uric Acid (PUA) in Patients with Type 1 Diabetes (T1D)
PUA is associated with renin angiotensin aldosterone system (RAAS) activation, which promotes hypertension and kidney disease in T1D. Our aims were to examine (1) the effect of an ANG II infusion on PUA and (2) the association between PUA and systemic and renal hemodynamic responses to ANG II over a...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2019-06, Vol.68 (Supplement_1) |
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| creator | LYTVYN, YULIYA LOVSHIN, JULIE A. BJORNSTAD, PETTER LOVBLOM, LEIF ERIK KATZ, ALEXANDRA LYTVYN, ANDRIY BOULET, GENEVIEVE FAROOQI, MOHAMMED A. WEISMAN, ALANNA KEENAN, HILLARY A. BRENT, MICHAEL H. PAUL, NARINDER BRIL, VERA ADVANI, ANDREW PERKINS, BRUCE A. CHERNEY, DAVID |
| description | PUA is associated with renin angiotensin aldosterone system (RAAS) activation, which promotes hypertension and kidney disease in T1D. Our aims were to examine (1) the effect of an ANG II infusion on PUA and (2) the association between PUA and systemic and renal hemodynamic responses to ANG II over a wide range of T1D duration.
In this post hoc analysis, blood pressure, PUA, GFRinulin and ERPFPAH were measured during a euglycemic clamp before and after an ANG II infusion (1 ng·kg-1·min-1) in participants with T1D: 49 young (26.2±5.5 years) and 62 older (66.0±7.9 years) adults and healthy controls (HC): 27 young (25.1±4.6 years), and 72 older (64.6±8.0 years) adults.
ANG II infusion caused a greater decline in GFRinulin in older vs. younger adults with T1D; there was no such difference between older vs. younger HC adults. ANG II decreased PUA more in HC than T1D in both age groups (p |
| doi_str_mv | 10.2337/db19-528-P |
| format | Article |
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In this post hoc analysis, blood pressure, PUA, GFRinulin and ERPFPAH were measured during a euglycemic clamp before and after an ANG II infusion (1 ng·kg-1·min-1) in participants with T1D: 49 young (26.2±5.5 years) and 62 older (66.0±7.9 years) adults and healthy controls (HC): 27 young (25.1±4.6 years), and 72 older (64.6±8.0 years) adults.
ANG II infusion caused a greater decline in GFRinulin in older vs. younger adults with T1D; there was no such difference between older vs. younger HC adults. ANG II decreased PUA more in HC than T1D in both age groups (p<0.0001, Figure 1). Decreases in PUA in response to ANG II infusion did not correlate with changes in renal or systemic hemodynamic parameters.
Our findings suggest that ANG II infusion reduces PUA, potentially through direct effects on the ANG II type 1 receptor (AT1R). The presence of T1D attenuates PUA lowering effects irrespective of diabetes duration, suggesting an interaction between hyperglycemia, RAAS signaling pathways and PUA. Further studies are required to better understand the effects of AT1R receptor signaling on PUA concentrations.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db19-528-P</identifier><language>eng</language><publisher>New York: American Diabetes Association</publisher><subject>Aldosterone ; Angiotensin ; Angiotensin II ; Blood pressure ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Hyperglycemia ; Kidney diseases ; Renin ; Uric acid</subject><ispartof>Diabetes (New York, N.Y.), 2019-06, Vol.68 (Supplement_1)</ispartof><rights>Copyright American Diabetes Association Jun 1, 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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></links><search><creatorcontrib>LYTVYN, YULIYA</creatorcontrib><creatorcontrib>LOVSHIN, JULIE A.</creatorcontrib><creatorcontrib>BJORNSTAD, PETTER</creatorcontrib><creatorcontrib>LOVBLOM, LEIF ERIK</creatorcontrib><creatorcontrib>KATZ, ALEXANDRA</creatorcontrib><creatorcontrib>LYTVYN, ANDRIY</creatorcontrib><creatorcontrib>BOULET, GENEVIEVE</creatorcontrib><creatorcontrib>FAROOQI, MOHAMMED A.</creatorcontrib><creatorcontrib>WEISMAN, ALANNA</creatorcontrib><creatorcontrib>KEENAN, HILLARY A.</creatorcontrib><creatorcontrib>BRENT, MICHAEL H.</creatorcontrib><creatorcontrib>PAUL, NARINDER</creatorcontrib><creatorcontrib>BRIL, VERA</creatorcontrib><creatorcontrib>ADVANI, ANDREW</creatorcontrib><creatorcontrib>PERKINS, BRUCE A.</creatorcontrib><creatorcontrib>CHERNEY, DAVID</creatorcontrib><title>528-P: The Effect of Angiotensin II (ANG II) Infusion on Plasma Uric Acid (PUA) in Patients with Type 1 Diabetes (T1D)</title><title>Diabetes (New York, N.Y.)</title><description>PUA is associated with renin angiotensin aldosterone system (RAAS) activation, which promotes hypertension and kidney disease in T1D. Our aims were to examine (1) the effect of an ANG II infusion on PUA and (2) the association between PUA and systemic and renal hemodynamic responses to ANG II over a wide range of T1D duration.
In this post hoc analysis, blood pressure, PUA, GFRinulin and ERPFPAH were measured during a euglycemic clamp before and after an ANG II infusion (1 ng·kg-1·min-1) in participants with T1D: 49 young (26.2±5.5 years) and 62 older (66.0±7.9 years) adults and healthy controls (HC): 27 young (25.1±4.6 years), and 72 older (64.6±8.0 years) adults.
ANG II infusion caused a greater decline in GFRinulin in older vs. younger adults with T1D; there was no such difference between older vs. younger HC adults. ANG II decreased PUA more in HC than T1D in both age groups (p<0.0001, Figure 1). Decreases in PUA in response to ANG II infusion did not correlate with changes in renal or systemic hemodynamic parameters.
Our findings suggest that ANG II infusion reduces PUA, potentially through direct effects on the ANG II type 1 receptor (AT1R). The presence of T1D attenuates PUA lowering effects irrespective of diabetes duration, suggesting an interaction between hyperglycemia, RAAS signaling pathways and PUA. Further studies are required to better understand the effects of AT1R receptor signaling on PUA concentrations.</description><subject>Aldosterone</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Blood pressure</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Hyperglycemia</subject><subject>Kidney diseases</subject><subject>Renin</subject><subject>Uric acid</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNotkF1LwzAUhoMoOKc3_oID3mxC9aRpm8a7ss05GNqLDrwLaZu4jK2dTafs35upnAPvzXM-eAi5pfgQMsYf65KKIA7TID8jAyqYCFjI38_JAJGGAeWCX5Ir5zaImPgakK9f-AmKtYaZMbrqoTWQNR-27XXjbAOLBYyy17nPMSwac3C2bcB3vlVup2DV2QqyytYwylfZGPxErnqrm97Bt-3XUBz3GihMrSp1rx2MCjodX5MLo7ZO3_znkBTPs2LyEizf5otJtgyqxP-eRCY2pWJUlCkTiQopVtygYmldI3KKRmvOBWVRjBEqFSWVKOM6QRrHqtY1G5K7v7X7rv08aNfLTXvoGn9RhmGURl5KIjx1_0dVXetcp43cd3anuqOkKE9a5Umr9KZkzn4A2qdlVw</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>LYTVYN, YULIYA</creator><creator>LOVSHIN, JULIE A.</creator><creator>BJORNSTAD, PETTER</creator><creator>LOVBLOM, LEIF ERIK</creator><creator>KATZ, ALEXANDRA</creator><creator>LYTVYN, ANDRIY</creator><creator>BOULET, GENEVIEVE</creator><creator>FAROOQI, MOHAMMED A.</creator><creator>WEISMAN, ALANNA</creator><creator>KEENAN, HILLARY A.</creator><creator>BRENT, MICHAEL H.</creator><creator>PAUL, NARINDER</creator><creator>BRIL, VERA</creator><creator>ADVANI, ANDREW</creator><creator>PERKINS, BRUCE A.</creator><creator>CHERNEY, DAVID</creator><general>American Diabetes Association</general><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20190601</creationdate><title>528-P: The Effect of Angiotensin II (ANG II) Infusion on Plasma Uric Acid (PUA) in Patients with Type 1 Diabetes (T1D)</title><author>LYTVYN, YULIYA ; LOVSHIN, JULIE A. ; BJORNSTAD, PETTER ; LOVBLOM, LEIF ERIK ; KATZ, ALEXANDRA ; LYTVYN, ANDRIY ; BOULET, GENEVIEVE ; FAROOQI, MOHAMMED A. ; WEISMAN, ALANNA ; KEENAN, HILLARY A. ; BRENT, MICHAEL H. ; PAUL, NARINDER ; BRIL, VERA ; ADVANI, ANDREW ; PERKINS, BRUCE A. ; CHERNEY, DAVID</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c639-64f5fba319b8396a210c7f0a38dd00710fee7791345040aa46c9b5d60155aded3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aldosterone</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Blood pressure</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Hyperglycemia</topic><topic>Kidney diseases</topic><topic>Renin</topic><topic>Uric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LYTVYN, YULIYA</creatorcontrib><creatorcontrib>LOVSHIN, JULIE A.</creatorcontrib><creatorcontrib>BJORNSTAD, PETTER</creatorcontrib><creatorcontrib>LOVBLOM, LEIF ERIK</creatorcontrib><creatorcontrib>KATZ, ALEXANDRA</creatorcontrib><creatorcontrib>LYTVYN, ANDRIY</creatorcontrib><creatorcontrib>BOULET, GENEVIEVE</creatorcontrib><creatorcontrib>FAROOQI, MOHAMMED A.</creatorcontrib><creatorcontrib>WEISMAN, ALANNA</creatorcontrib><creatorcontrib>KEENAN, HILLARY A.</creatorcontrib><creatorcontrib>BRENT, MICHAEL H.</creatorcontrib><creatorcontrib>PAUL, NARINDER</creatorcontrib><creatorcontrib>BRIL, VERA</creatorcontrib><creatorcontrib>ADVANI, ANDREW</creatorcontrib><creatorcontrib>PERKINS, BRUCE A.</creatorcontrib><creatorcontrib>CHERNEY, DAVID</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LYTVYN, YULIYA</au><au>LOVSHIN, JULIE A.</au><au>BJORNSTAD, PETTER</au><au>LOVBLOM, LEIF ERIK</au><au>KATZ, ALEXANDRA</au><au>LYTVYN, ANDRIY</au><au>BOULET, GENEVIEVE</au><au>FAROOQI, MOHAMMED A.</au><au>WEISMAN, ALANNA</au><au>KEENAN, HILLARY A.</au><au>BRENT, MICHAEL H.</au><au>PAUL, NARINDER</au><au>BRIL, VERA</au><au>ADVANI, ANDREW</au><au>PERKINS, BRUCE A.</au><au>CHERNEY, DAVID</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>528-P: The Effect of Angiotensin II (ANG II) Infusion on Plasma Uric Acid (PUA) in Patients with Type 1 Diabetes (T1D)</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><date>2019-06-01</date><risdate>2019</risdate><volume>68</volume><issue>Supplement_1</issue><issn>0012-1797</issn><eissn>1939-327X</eissn><abstract>PUA is associated with renin angiotensin aldosterone system (RAAS) activation, which promotes hypertension and kidney disease in T1D. Our aims were to examine (1) the effect of an ANG II infusion on PUA and (2) the association between PUA and systemic and renal hemodynamic responses to ANG II over a wide range of T1D duration.
In this post hoc analysis, blood pressure, PUA, GFRinulin and ERPFPAH were measured during a euglycemic clamp before and after an ANG II infusion (1 ng·kg-1·min-1) in participants with T1D: 49 young (26.2±5.5 years) and 62 older (66.0±7.9 years) adults and healthy controls (HC): 27 young (25.1±4.6 years), and 72 older (64.6±8.0 years) adults.
ANG II infusion caused a greater decline in GFRinulin in older vs. younger adults with T1D; there was no such difference between older vs. younger HC adults. ANG II decreased PUA more in HC than T1D in both age groups (p<0.0001, Figure 1). Decreases in PUA in response to ANG II infusion did not correlate with changes in renal or systemic hemodynamic parameters.
Our findings suggest that ANG II infusion reduces PUA, potentially through direct effects on the ANG II type 1 receptor (AT1R). The presence of T1D attenuates PUA lowering effects irrespective of diabetes duration, suggesting an interaction between hyperglycemia, RAAS signaling pathways and PUA. Further studies are required to better understand the effects of AT1R receptor signaling on PUA concentrations.</abstract><cop>New York</cop><pub>American Diabetes Association</pub><doi>10.2337/db19-528-P</doi></addata></record> |
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| language | eng |
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| source | EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Aldosterone Angiotensin Angiotensin II Blood pressure Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Hyperglycemia Kidney diseases Renin Uric acid |
| title | 528-P: The Effect of Angiotensin II (ANG II) Infusion on Plasma Uric Acid (PUA) in Patients with Type 1 Diabetes (T1D) |
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