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Insulin resistance is affected by sodium intake in nonmodulating subset of essential hypertension
Insulin resistance (IR) is one of the possible causes of essential hypertension (EH). Relationship between IR and pathophysiologic mechanisms are poorly understood, although an association between salt sensitive EH and IR has been reported. The purpose of this study was to determine if IR measured u...
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Published in: | American journal of hypertension 2000-04, Vol.13 (4), p.8A-8A |
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description | Insulin resistance (IR) is one of the possible causes of essential hypertension (EH). Relationship between IR and pathophysiologic mechanisms are poorly understood, although an association between salt sensitive EH and IR has been reported. The purpose of this study was to determine if IR measured using homeostasis model assessment (HOMA) was a) different in subsets of EH determined according to the abnormalities in the renin-angiotensin system: Low renin, Non-modulators (NM), and Modulators. The latter two are normal/high renin group. b) Modified by the level of sodium (Na) intake in the different subsets. Fasting insulin and glucose were determined in subsets of EH and normotensives (NT) and HOMA was calculated as fasting glucose (mmol)* fasting insulin (μmol)/22.5, and was log transformed for analysis. ANOVA, paired t and non-parametric tests were used to compare subsets. EH (N=265) as a whole had significantly higher fasting insulin (p |
doi_str_mv | 10.1016/S0895-7061(00)00320-4 |
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Relationship between IR and pathophysiologic mechanisms are poorly understood, although an association between salt sensitive EH and IR has been reported. The purpose of this study was to determine if IR measured using homeostasis model assessment (HOMA) was a) different in subsets of EH determined according to the abnormalities in the renin-angiotensin system: Low renin, Non-modulators (NM), and Modulators. The latter two are normal/high renin group. b) Modified by the level of sodium (Na) intake in the different subsets. Fasting insulin and glucose were determined in subsets of EH and normotensives (NT) and HOMA was calculated as fasting glucose (mmol)* fasting insulin (μmol)/22.5, and was log transformed for analysis. ANOVA, paired t and non-parametric tests were used to compare subsets. EH (N=265) as a whole had significantly higher fasting insulin (p<.001) and HOMA (p<.001) on low Na than NT. Within the EH subsets the NM had the highest fasting insulin levels and HOMA, with further increase in HOMA on low Na (Table). This was independent of the potential confounders of BMI, race and age. Black NM (n = 18) did not show significant change in HOMA (p = .982) or fasting insulin (p = .782) with low Na. HOMA N Low Na High Na Nonmodulators 58 6.12* 4.00 Modulators 129 4.30 3.54 Low Renin 54 2.84 2.24 Normotensives 21 3.84 2.60 *p<0.005 NM are more IR than other subsets of EH. 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Relationship between IR and pathophysiologic mechanisms are poorly understood, although an association between salt sensitive EH and IR has been reported. The purpose of this study was to determine if IR measured using homeostasis model assessment (HOMA) was a) different in subsets of EH determined according to the abnormalities in the renin-angiotensin system: Low renin, Non-modulators (NM), and Modulators. The latter two are normal/high renin group. b) Modified by the level of sodium (Na) intake in the different subsets. Fasting insulin and glucose were determined in subsets of EH and normotensives (NT) and HOMA was calculated as fasting glucose (mmol)* fasting insulin (μmol)/22.5, and was log transformed for analysis. ANOVA, paired t and non-parametric tests were used to compare subsets. EH (N=265) as a whole had significantly higher fasting insulin (p<.001) and HOMA (p<.001) on low Na than NT. Within the EH subsets the NM had the highest fasting insulin levels and HOMA, with further increase in HOMA on low Na (Table). This was independent of the potential confounders of BMI, race and age. Black NM (n = 18) did not show significant change in HOMA (p = .982) or fasting insulin (p = .782) with low Na. HOMA N Low Na High Na Nonmodulators 58 6.12* 4.00 Modulators 129 4.30 3.54 Low Renin 54 2.84 2.24 Normotensives 21 3.84 2.60 *p<0.005 NM are more IR than other subsets of EH. In Caucasians, but not in Blacks, low Na intake leads to an further increase in IR in NM, an effect not seen in other EH subgroups or NT.</description><subject>Essential hypertension</subject><subject>Insulin resistance</subject><subject>nonmodulators</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqFkU1v1DAQhi1EJZbCT0CyxAUOgXHij-SEaAVspaIe2kqIi-XYE-rtrr3YDmL_Pd4GlSOnOcwz74yeIeQVg3cMmHx_Df0gGgWSvQF4C9C10PAnZMV6NTRsAPGUrB6RZ-R5zhsA4FKyFTEXIc9bH2jC7HMxwSL1mZppQlvQ0fFAc3R-3lEfirmvzUBDDLvo5q0pPvygeR4zFhonijljKN5s6d1hj6lgyD6GF-RkMtuML__WU3L7-dPN-bq5vPpycf7xsrEtB95IpYwZ3Tj0xsFouQM5SGxbi1JYY_jEUDGU0nB0o3CTEq6dLJpx5Ax75N0peb3k7lP8OWMuehPnFOpKzaDrmRCtGiolFsqmmHPCSe-T35l0qJA-2tQPNvVRlQbQDzb1MZ0uc8GUOeHjlNnctVVm2x2jmwWpHvH3PyLda6k6JfT623d9rdRXtj6T-qzyHxYeq5VfHpPO1mN9gPOpytcu-v8c9QcKDpjN</recordid><startdate>20000401</startdate><enddate>20000401</enddate><creator>Raji, A.</creator><creator>Williams, G.H.</creator><creator>Xavier, J.</creator><creator>Hopkins, P.N.</creator><creator>Hunt, S.C.</creator><creator>Hollenberg, N.K.</creator><creator>Seely, E.W.</creator><general>Elsevier Inc</general><general>Oxford University Press</general><scope>BSCLL</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20000401</creationdate><title>Insulin resistance is affected by sodium intake in nonmodulating subset of essential hypertension</title><author>Raji, A. ; Williams, G.H. ; Xavier, J. ; Hopkins, P.N. ; Hunt, S.C. ; Hollenberg, N.K. ; Seely, E.W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2404-677aabdb98ad0bc4d0696e22ce65caa4f1e71e66a4edb5df75d2fceabb41e8e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Essential hypertension</topic><topic>Insulin resistance</topic><topic>nonmodulators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Raji, A.</creatorcontrib><creatorcontrib>Williams, G.H.</creatorcontrib><creatorcontrib>Xavier, J.</creatorcontrib><creatorcontrib>Hopkins, P.N.</creatorcontrib><creatorcontrib>Hunt, S.C.</creatorcontrib><creatorcontrib>Hollenberg, N.K.</creatorcontrib><creatorcontrib>Seely, E.W.</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>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><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Raji, A.</au><au>Williams, G.H.</au><au>Xavier, J.</au><au>Hopkins, P.N.</au><au>Hunt, S.C.</au><au>Hollenberg, N.K.</au><au>Seely, E.W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin resistance is affected by sodium intake in nonmodulating subset of essential hypertension</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2000-04-01</date><risdate>2000</risdate><volume>13</volume><issue>4</issue><spage>8A</spage><epage>8A</epage><pages>8A-8A</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>Insulin resistance (IR) is one of the possible causes of essential hypertension (EH). Relationship between IR and pathophysiologic mechanisms are poorly understood, although an association between salt sensitive EH and IR has been reported. The purpose of this study was to determine if IR measured using homeostasis model assessment (HOMA) was a) different in subsets of EH determined according to the abnormalities in the renin-angiotensin system: Low renin, Non-modulators (NM), and Modulators. The latter two are normal/high renin group. b) Modified by the level of sodium (Na) intake in the different subsets. Fasting insulin and glucose were determined in subsets of EH and normotensives (NT) and HOMA was calculated as fasting glucose (mmol)* fasting insulin (μmol)/22.5, and was log transformed for analysis. ANOVA, paired t and non-parametric tests were used to compare subsets. EH (N=265) as a whole had significantly higher fasting insulin (p<.001) and HOMA (p<.001) on low Na than NT. Within the EH subsets the NM had the highest fasting insulin levels and HOMA, with further increase in HOMA on low Na (Table). This was independent of the potential confounders of BMI, race and age. Black NM (n = 18) did not show significant change in HOMA (p = .982) or fasting insulin (p = .782) with low Na. HOMA N Low Na High Na Nonmodulators 58 6.12* 4.00 Modulators 129 4.30 3.54 Low Renin 54 2.84 2.24 Normotensives 21 3.84 2.60 *p<0.005 NM are more IR than other subsets of EH. In Caucasians, but not in Blacks, low Na intake leads to an further increase in IR in NM, an effect not seen in other EH subgroups or NT.</abstract><cop>Oxford</cop><pub>Elsevier Inc</pub><doi>10.1016/S0895-7061(00)00320-4</doi><oa>free_for_read</oa></addata></record> |
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title | Insulin resistance is affected by sodium intake in nonmodulating subset of essential hypertension |
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