1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA)
Elevated SNSA induces dysglycemia by enhancing adipose lipolysis and stimulating hepatic glucose production. It also promotes cardiovascular disease (CVD) by multiple mechanisms including augmenting systemic and vascular reactive oxygen and nitrogen species (ROS, RNS) generation. Elevated plasma pro...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2019-06, Vol.68 (Supplement_1) |
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| creator | CHAMARTHI, BINDU CERSOSIMO, EUGENIO ADAMS, JOHN M. ALATRACH, MARIAM AGYIN, CHRISTINA TRIPLITT, CURTIS L. EZROKHI, MICHAEL LUO, SHUQIN DUVALLET, EMILIE CINCOTTA, ANTHONY H. DEFRONZO, RALPH A. |
| description | Elevated SNSA induces dysglycemia by enhancing adipose lipolysis and stimulating hepatic glucose production. It also promotes cardiovascular disease (CVD) by multiple mechanisms including augmenting systemic and vascular reactive oxygen and nitrogen species (ROS, RNS) generation. Elevated plasma prolactin (subclinical hyperprolactinemia) has also been associated with systemic inflammation, which can potentiate dysglycemia and CVD. BQR, the only dopamine agonist approved for treatment of T2D, improves postprandial dysglycemia and reduces CVD events. To evaluate mechanisms for the glucose lowering and CVD protective effects of BQR, we evaluated BQR’s effect on plasma markers of SNSA and ROS/RNS and plasma prolactin and leptin from a mechanistic study in which BQR added to 15 T2D subjects (HbA1c 8.3%) treated with a GLP-1 RA significantly improved HbA1c (-0.6%), postprandial hyperglycemia (by 22%) and endothelial dysfunction (by 36%). Plasma norepinephrine (NE), normetanephrine (NM), TBAR (a marker of systemic OS), nitrotyrosine (NT, a marker of systemic oxidative/nitrosative stress), prolactin and leptin were measured at baseline and after 4 months of BQR add-on therapy (3.2 mg/day). Plasma NE, NM, TBAR, NT and prolactin levels were elevated at baseline and decreased significantly with BQR [NE by 33% (2.95 to 1.95 ng/mL, p |
| doi_str_mv | 10.2337/db19-1166-P |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2248398706</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2248398706</sourcerecordid><originalsourceid>FETCH-LOGICAL-c646-8538d25f1aac04e093f8c6e1a7f0d2a14409226f82f70c6535b6820ff0af50063</originalsourceid><addsrcrecordid>eNotkc2O00AQhC0EEmHhxAu0xMUWMsyPf7llk2VZKdpkYx-4WZNxezOR7TEz44AfmbfA2aA-tFT61FXq8ryPlHxhnKdf6wPNQ0qTJNy98hY053nIWfrztbcghLKQpnn61ntn7YkQksyz8P5e6W9wa3SnpVGDUz2GT3vwb5_2AZRHNGKYYI_1KNHCXYtn4bCGYuoG4Y7olIRHNGc92lmzDjtYSqfOyk3gF4_FMgDR17D9o2oxywiFM2gt-NsiANVDOQ0IDNZKHNDNBn7J1gEU4-GE0ln4fdQWYT3Z53aS2CkBDxZ2Wpt2gpXundFtO6fRPdxvdiGdc0ocnDawfNa9sg78F32_DN57bxrRWvzwf9945fe7cvUj3GzvH1bLTSiTKAmzmGc1ixsqhCQRkpw3mUyQirQhNRM0ikjOWNJkrEmJTGIeH5KMkaYhoonnp_Ib79P17GD0rxGtq056NP3sWDEWZTzP0hfq85WSRltrsKkGozphpoqS6lJldamyupRT7fg_ThuPbg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2248398706</pqid></control><display><type>article</type><title>1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA)</title><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>CHAMARTHI, BINDU ; CERSOSIMO, EUGENIO ; ADAMS, JOHN M. ; ALATRACH, MARIAM ; AGYIN, CHRISTINA ; TRIPLITT, CURTIS L. ; EZROKHI, MICHAEL ; LUO, SHUQIN ; DUVALLET, EMILIE ; CINCOTTA, ANTHONY H. ; DEFRONZO, RALPH A.</creator><creatorcontrib>CHAMARTHI, BINDU ; CERSOSIMO, EUGENIO ; ADAMS, JOHN M. ; ALATRACH, MARIAM ; AGYIN, CHRISTINA ; TRIPLITT, CURTIS L. ; EZROKHI, MICHAEL ; LUO, SHUQIN ; DUVALLET, EMILIE ; CINCOTTA, ANTHONY H. ; DEFRONZO, RALPH A.</creatorcontrib><description>Elevated SNSA induces dysglycemia by enhancing adipose lipolysis and stimulating hepatic glucose production. It also promotes cardiovascular disease (CVD) by multiple mechanisms including augmenting systemic and vascular reactive oxygen and nitrogen species (ROS, RNS) generation. Elevated plasma prolactin (subclinical hyperprolactinemia) has also been associated with systemic inflammation, which can potentiate dysglycemia and CVD. BQR, the only dopamine agonist approved for treatment of T2D, improves postprandial dysglycemia and reduces CVD events. To evaluate mechanisms for the glucose lowering and CVD protective effects of BQR, we evaluated BQR’s effect on plasma markers of SNSA and ROS/RNS and plasma prolactin and leptin from a mechanistic study in which BQR added to 15 T2D subjects (HbA1c 8.3%) treated with a GLP-1 RA significantly improved HbA1c (-0.6%), postprandial hyperglycemia (by 22%) and endothelial dysfunction (by 36%). Plasma norepinephrine (NE), normetanephrine (NM), TBAR (a marker of systemic OS), nitrotyrosine (NT, a marker of systemic oxidative/nitrosative stress), prolactin and leptin were measured at baseline and after 4 months of BQR add-on therapy (3.2 mg/day). Plasma NE, NM, TBAR, NT and prolactin levels were elevated at baseline and decreased significantly with BQR [NE by 33% (2.95 to 1.95 ng/mL, p <0.0005); NM by 22% (56.5 to 44.3 pg/ml, p<0.018); TBAR by 10% (10.2 to 9.2 μM, p=0.04); NT by 13% (214 to 187 nM, p<0.02); prolactin by 42% (13.0 to 7.6 ng/ml, p<0.012)]. Plasma leptin, unchanged in the whole group, decreased 23% (35.7 to 27.5 ng/mL, p=0.038) in subjects with elevated leptin (>20 ng/dl, N=7) at baseline.
Conclusion: Bromocriptine-QR is the only T2D therapy known to simultaneously reduce elevated plasma NE, NM, prolactin and OS and such actions may be important for the drug’s glucose lowering and CVD protective effects.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db19-1166-P</identifier><language>eng</language><publisher>New York: American Diabetes Association</publisher><subject>Agonists ; Bromocriptine ; Cardiovascular diseases ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Dopamine ; GLP-1 receptor agonists ; Glucose ; Hyperglycemia ; Hyperprolactinemia ; Leptin ; Lipolysis ; Nitrotyrosine ; Norepinephrine ; Oxidative stress ; Prolactin ; Reactive oxygen species ; Sympathetic nervous system</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>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>CHAMARTHI, BINDU</creatorcontrib><creatorcontrib>CERSOSIMO, EUGENIO</creatorcontrib><creatorcontrib>ADAMS, JOHN M.</creatorcontrib><creatorcontrib>ALATRACH, MARIAM</creatorcontrib><creatorcontrib>AGYIN, CHRISTINA</creatorcontrib><creatorcontrib>TRIPLITT, CURTIS L.</creatorcontrib><creatorcontrib>EZROKHI, MICHAEL</creatorcontrib><creatorcontrib>LUO, SHUQIN</creatorcontrib><creatorcontrib>DUVALLET, EMILIE</creatorcontrib><creatorcontrib>CINCOTTA, ANTHONY H.</creatorcontrib><creatorcontrib>DEFRONZO, RALPH A.</creatorcontrib><title>1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA)</title><title>Diabetes (New York, N.Y.)</title><description>Elevated SNSA induces dysglycemia by enhancing adipose lipolysis and stimulating hepatic glucose production. It also promotes cardiovascular disease (CVD) by multiple mechanisms including augmenting systemic and vascular reactive oxygen and nitrogen species (ROS, RNS) generation. Elevated plasma prolactin (subclinical hyperprolactinemia) has also been associated with systemic inflammation, which can potentiate dysglycemia and CVD. BQR, the only dopamine agonist approved for treatment of T2D, improves postprandial dysglycemia and reduces CVD events. To evaluate mechanisms for the glucose lowering and CVD protective effects of BQR, we evaluated BQR’s effect on plasma markers of SNSA and ROS/RNS and plasma prolactin and leptin from a mechanistic study in which BQR added to 15 T2D subjects (HbA1c 8.3%) treated with a GLP-1 RA significantly improved HbA1c (-0.6%), postprandial hyperglycemia (by 22%) and endothelial dysfunction (by 36%). Plasma norepinephrine (NE), normetanephrine (NM), TBAR (a marker of systemic OS), nitrotyrosine (NT, a marker of systemic oxidative/nitrosative stress), prolactin and leptin were measured at baseline and after 4 months of BQR add-on therapy (3.2 mg/day). Plasma NE, NM, TBAR, NT and prolactin levels were elevated at baseline and decreased significantly with BQR [NE by 33% (2.95 to 1.95 ng/mL, p <0.0005); NM by 22% (56.5 to 44.3 pg/ml, p<0.018); TBAR by 10% (10.2 to 9.2 μM, p=0.04); NT by 13% (214 to 187 nM, p<0.02); prolactin by 42% (13.0 to 7.6 ng/ml, p<0.012)]. Plasma leptin, unchanged in the whole group, decreased 23% (35.7 to 27.5 ng/mL, p=0.038) in subjects with elevated leptin (>20 ng/dl, N=7) at baseline.
Conclusion: Bromocriptine-QR is the only T2D therapy known to simultaneously reduce elevated plasma NE, NM, prolactin and OS and such actions may be important for the drug’s glucose lowering and CVD protective effects.</description><subject>Agonists</subject><subject>Bromocriptine</subject><subject>Cardiovascular diseases</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Dopamine</subject><subject>GLP-1 receptor agonists</subject><subject>Glucose</subject><subject>Hyperglycemia</subject><subject>Hyperprolactinemia</subject><subject>Leptin</subject><subject>Lipolysis</subject><subject>Nitrotyrosine</subject><subject>Norepinephrine</subject><subject>Oxidative stress</subject><subject>Prolactin</subject><subject>Reactive oxygen species</subject><subject>Sympathetic nervous system</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNotkc2O00AQhC0EEmHhxAu0xMUWMsyPf7llk2VZKdpkYx-4WZNxezOR7TEz44AfmbfA2aA-tFT61FXq8ryPlHxhnKdf6wPNQ0qTJNy98hY053nIWfrztbcghLKQpnn61ntn7YkQksyz8P5e6W9wa3SnpVGDUz2GT3vwb5_2AZRHNGKYYI_1KNHCXYtn4bCGYuoG4Y7olIRHNGc92lmzDjtYSqfOyk3gF4_FMgDR17D9o2oxywiFM2gt-NsiANVDOQ0IDNZKHNDNBn7J1gEU4-GE0ln4fdQWYT3Z53aS2CkBDxZ2Wpt2gpXundFtO6fRPdxvdiGdc0ocnDawfNa9sg78F32_DN57bxrRWvzwf9945fe7cvUj3GzvH1bLTSiTKAmzmGc1ixsqhCQRkpw3mUyQirQhNRM0ikjOWNJkrEmJTGIeH5KMkaYhoonnp_Ib79P17GD0rxGtq056NP3sWDEWZTzP0hfq85WSRltrsKkGozphpoqS6lJldamyupRT7fg_ThuPbg</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>CHAMARTHI, BINDU</creator><creator>CERSOSIMO, EUGENIO</creator><creator>ADAMS, JOHN M.</creator><creator>ALATRACH, MARIAM</creator><creator>AGYIN, CHRISTINA</creator><creator>TRIPLITT, CURTIS L.</creator><creator>EZROKHI, MICHAEL</creator><creator>LUO, SHUQIN</creator><creator>DUVALLET, EMILIE</creator><creator>CINCOTTA, ANTHONY H.</creator><creator>DEFRONZO, RALPH A.</creator><general>American Diabetes Association</general><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20190601</creationdate><title>1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA)</title><author>CHAMARTHI, BINDU ; CERSOSIMO, EUGENIO ; ADAMS, JOHN M. ; ALATRACH, MARIAM ; AGYIN, CHRISTINA ; TRIPLITT, CURTIS L. ; EZROKHI, MICHAEL ; LUO, SHUQIN ; DUVALLET, EMILIE ; CINCOTTA, ANTHONY H. ; DEFRONZO, RALPH A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c646-8538d25f1aac04e093f8c6e1a7f0d2a14409226f82f70c6535b6820ff0af50063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Agonists</topic><topic>Bromocriptine</topic><topic>Cardiovascular diseases</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Dopamine</topic><topic>GLP-1 receptor agonists</topic><topic>Glucose</topic><topic>Hyperglycemia</topic><topic>Hyperprolactinemia</topic><topic>Leptin</topic><topic>Lipolysis</topic><topic>Nitrotyrosine</topic><topic>Norepinephrine</topic><topic>Oxidative stress</topic><topic>Prolactin</topic><topic>Reactive oxygen species</topic><topic>Sympathetic nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHAMARTHI, BINDU</creatorcontrib><creatorcontrib>CERSOSIMO, EUGENIO</creatorcontrib><creatorcontrib>ADAMS, JOHN M.</creatorcontrib><creatorcontrib>ALATRACH, MARIAM</creatorcontrib><creatorcontrib>AGYIN, CHRISTINA</creatorcontrib><creatorcontrib>TRIPLITT, CURTIS L.</creatorcontrib><creatorcontrib>EZROKHI, MICHAEL</creatorcontrib><creatorcontrib>LUO, SHUQIN</creatorcontrib><creatorcontrib>DUVALLET, EMILIE</creatorcontrib><creatorcontrib>CINCOTTA, ANTHONY H.</creatorcontrib><creatorcontrib>DEFRONZO, RALPH A.</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>CHAMARTHI, BINDU</au><au>CERSOSIMO, EUGENIO</au><au>ADAMS, JOHN M.</au><au>ALATRACH, MARIAM</au><au>AGYIN, CHRISTINA</au><au>TRIPLITT, CURTIS L.</au><au>EZROKHI, MICHAEL</au><au>LUO, SHUQIN</au><au>DUVALLET, EMILIE</au><au>CINCOTTA, ANTHONY H.</au><au>DEFRONZO, RALPH A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA)</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>Elevated SNSA induces dysglycemia by enhancing adipose lipolysis and stimulating hepatic glucose production. It also promotes cardiovascular disease (CVD) by multiple mechanisms including augmenting systemic and vascular reactive oxygen and nitrogen species (ROS, RNS) generation. Elevated plasma prolactin (subclinical hyperprolactinemia) has also been associated with systemic inflammation, which can potentiate dysglycemia and CVD. BQR, the only dopamine agonist approved for treatment of T2D, improves postprandial dysglycemia and reduces CVD events. To evaluate mechanisms for the glucose lowering and CVD protective effects of BQR, we evaluated BQR’s effect on plasma markers of SNSA and ROS/RNS and plasma prolactin and leptin from a mechanistic study in which BQR added to 15 T2D subjects (HbA1c 8.3%) treated with a GLP-1 RA significantly improved HbA1c (-0.6%), postprandial hyperglycemia (by 22%) and endothelial dysfunction (by 36%). Plasma norepinephrine (NE), normetanephrine (NM), TBAR (a marker of systemic OS), nitrotyrosine (NT, a marker of systemic oxidative/nitrosative stress), prolactin and leptin were measured at baseline and after 4 months of BQR add-on therapy (3.2 mg/day). Plasma NE, NM, TBAR, NT and prolactin levels were elevated at baseline and decreased significantly with BQR [NE by 33% (2.95 to 1.95 ng/mL, p <0.0005); NM by 22% (56.5 to 44.3 pg/ml, p<0.018); TBAR by 10% (10.2 to 9.2 μM, p=0.04); NT by 13% (214 to 187 nM, p<0.02); prolactin by 42% (13.0 to 7.6 ng/ml, p<0.012)]. Plasma leptin, unchanged in the whole group, decreased 23% (35.7 to 27.5 ng/mL, p=0.038) in subjects with elevated leptin (>20 ng/dl, N=7) at baseline.
Conclusion: Bromocriptine-QR is the only T2D therapy known to simultaneously reduce elevated plasma NE, NM, prolactin and OS and such actions may be important for the drug’s glucose lowering and CVD protective effects.</abstract><cop>New York</cop><pub>American Diabetes Association</pub><doi>10.2337/db19-1166-P</doi></addata></record> |
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| subjects | Agonists Bromocriptine Cardiovascular diseases Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Dopamine GLP-1 receptor agonists Glucose Hyperglycemia Hyperprolactinemia Leptin Lipolysis Nitrotyrosine Norepinephrine Oxidative stress Prolactin Reactive oxygen species Sympathetic nervous system |
| title | 1166-P: Bromocriptine-QR (BQR) Therapy Reduces Elevated Sympathetic Nervous System Activity (SNSA) and Oxidative Stress (OS) in Type 2 Diabetes (T2D) Subjects whose Dysglycemia Is Poorly Controlled on GLP-1 Receptor Agonist (GLP-1RA) |
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