Genetic variations in magnesium-related ion channels may affect diabetes risk among African American and Hispanic American women
Prospective studies consistently link low magnesium intake to higher type 2 diabetes (T2D) risk. We examined the association of common genetic variants [single nucleotide polymorphisms (SNPs)] in genes related to magnesium homeostasis with T2D risk and potential interactions with magnesium intake. U...
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| Veröffentlicht in: | The Journal of nutrition 2015-03, Vol.145 (3), p.418-424 |
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| creator | Chan, Kei Hang K Chacko, Sara A Song, Yiqing Cho, Michele Eaton, Charles B Wu, Wen-Chih H Liu, Simin |
| description | Prospective studies consistently link low magnesium intake to higher type 2 diabetes (T2D) risk.
We examined the association of common genetic variants [single nucleotide polymorphisms (SNPs)] in genes related to magnesium homeostasis with T2D risk and potential interactions with magnesium intake.
Using the Women's Health Initiative-SNP Health Association Resource (WHI-SHARe) study, we identified 17 magnesium-related ion channel genes (583 SNPs) and examined their associations with T2D risk in 7287 African-American (AA; n = 1949 T2D cases) and 3285 Hispanic-American (HA; n = 611 T2D cases) postmenopausal women. We performed both single- and multiple-locus haplotype analyses.
Among AA women, carriers of each additional copy of SNP rs6584273 in cyclin mediator 1 (CNNM1) had 16% lower T2D risk [OR: 0.84; false discovery rate (FDR)-adjusted P = 0.02]. Among HA women, several variants were significantly associated with T2D risk, including rs10861279 in solute carrier family 41 (anion exchanger), member 2 (SLC41A2) (OR: 0.54; FDR-adjusted P = 0.04), rs7174119 in nonimprinted in Prader-Willi/Angelman syndrome 1 (NIPA1) (OR: 1.27; FDR-adjusted P = 0.04), and 2 SNPs in mitochondrial RNA splicing 2 (MRS2) (rs7738943: OR = 1.55, FDR-adjusted P = 0.01; rs1056285: OR = 1.48, FDR-adjusted P = 0.02). Even with the most conservative Bonferroni adjustment, two 2-SNP-haplotypes in SLC41A2 and MRS2 region were significantly associated with T2D risk (rs12582312-rs10861279: P = 0.0006; rs1056285-rs7738943: P = 0.002). Among women with magnesium intake in the lowest 30% (AA: ≤0.164 g/d; HA: ≤0.185 g/d), 4 SNP signals were strengthened [rs11590362 in claudin 19 (CLDN19), rs823154 in SLC41A1, rs5929706 and rs5930817 in membra; HA: ≥0.313 g/d), rs6584273 in CNNM1 (OR: 0.71; FDR-adjusted P = 0.04) and rs1800467 in potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) (OR: 2.50; FDR-adjusted P = 0.01) were significantly associated with T2D risk.
Our findings suggest important associations between genetic variations in magnesium-related ion channel genes and T2D risk in AA and HA women that vary by amount of magnesium intake. |
| doi_str_mv | 10.3945/jn.114.203489 |
| format | Article |
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We examined the association of common genetic variants [single nucleotide polymorphisms (SNPs)] in genes related to magnesium homeostasis with T2D risk and potential interactions with magnesium intake.
Using the Women's Health Initiative-SNP Health Association Resource (WHI-SHARe) study, we identified 17 magnesium-related ion channel genes (583 SNPs) and examined their associations with T2D risk in 7287 African-American (AA; n = 1949 T2D cases) and 3285 Hispanic-American (HA; n = 611 T2D cases) postmenopausal women. We performed both single- and multiple-locus haplotype analyses.
Among AA women, carriers of each additional copy of SNP rs6584273 in cyclin mediator 1 (CNNM1) had 16% lower T2D risk [OR: 0.84; false discovery rate (FDR)-adjusted P = 0.02]. Among HA women, several variants were significantly associated with T2D risk, including rs10861279 in solute carrier family 41 (anion exchanger), member 2 (SLC41A2) (OR: 0.54; FDR-adjusted P = 0.04), rs7174119 in nonimprinted in Prader-Willi/Angelman syndrome 1 (NIPA1) (OR: 1.27; FDR-adjusted P = 0.04), and 2 SNPs in mitochondrial RNA splicing 2 (MRS2) (rs7738943: OR = 1.55, FDR-adjusted P = 0.01; rs1056285: OR = 1.48, FDR-adjusted P = 0.02). Even with the most conservative Bonferroni adjustment, two 2-SNP-haplotypes in SLC41A2 and MRS2 region were significantly associated with T2D risk (rs12582312-rs10861279: P = 0.0006; rs1056285-rs7738943: P = 0.002). Among women with magnesium intake in the lowest 30% (AA: ≤0.164 g/d; HA: ≤0.185 g/d), 4 SNP signals were strengthened [rs11590362 in claudin 19 (CLDN19), rs823154 in SLC41A1, rs5929706 and rs5930817 in membra; HA: ≥0.313 g/d), rs6584273 in CNNM1 (OR: 0.71; FDR-adjusted P = 0.04) and rs1800467 in potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) (OR: 2.50; FDR-adjusted P = 0.01) were significantly associated with T2D risk.
Our findings suggest important associations between genetic variations in magnesium-related ion channel genes and T2D risk in AA and HA women that vary by amount of magnesium intake.</description><identifier>ISSN: 0022-3166</identifier><identifier>EISSN: 1541-6100</identifier><identifier>DOI: 10.3945/jn.114.203489</identifier><identifier>PMID: 25733456</identifier><language>eng</language><publisher>United States: American Society for Nutrition</publisher><subject>Aged ; Biochemical, Molecular, and Genetic Mechanisms ; Black or African American - genetics ; Body Mass Index ; Case-Control Studies ; Cation Transport Proteins - genetics ; Claudins - genetics ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Dietary Supplements ; Female ; Genetic Loci ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotyping Techniques ; Haplotypes ; Hispanic or Latino - genetics ; Humans ; Ion Channels - genetics ; Logistic Models ; Magnesium - administration & dosage ; Magnesium - blood ; Middle Aged ; Polymorphism, Single Nucleotide ; Postmenopause ; Potassium Channels, Inwardly Rectifying - genetics ; Prospective Studies ; Risk Factors</subject><ispartof>The Journal of nutrition, 2015-03, Vol.145 (3), p.418-424</ispartof><rights>2015 American Society for Nutrition.</rights><rights>2015 American Society for Nutrition 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-8b68d9af6faa04f152dd9ea3d1dcd7e8fb680b3a90f98b4baa22dcc026d8f8e3</citedby><cites>FETCH-LOGICAL-c453t-8b68d9af6faa04f152dd9ea3d1dcd7e8fb680b3a90f98b4baa22dcc026d8f8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25733456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chan, Kei Hang K</creatorcontrib><creatorcontrib>Chacko, Sara A</creatorcontrib><creatorcontrib>Song, Yiqing</creatorcontrib><creatorcontrib>Cho, Michele</creatorcontrib><creatorcontrib>Eaton, Charles B</creatorcontrib><creatorcontrib>Wu, Wen-Chih H</creatorcontrib><creatorcontrib>Liu, Simin</creatorcontrib><title>Genetic variations in magnesium-related ion channels may affect diabetes risk among African American and Hispanic American women</title><title>The Journal of nutrition</title><addtitle>J Nutr</addtitle><description>Prospective studies consistently link low magnesium intake to higher type 2 diabetes (T2D) risk.
We examined the association of common genetic variants [single nucleotide polymorphisms (SNPs)] in genes related to magnesium homeostasis with T2D risk and potential interactions with magnesium intake.
Using the Women's Health Initiative-SNP Health Association Resource (WHI-SHARe) study, we identified 17 magnesium-related ion channel genes (583 SNPs) and examined their associations with T2D risk in 7287 African-American (AA; n = 1949 T2D cases) and 3285 Hispanic-American (HA; n = 611 T2D cases) postmenopausal women. We performed both single- and multiple-locus haplotype analyses.
Among AA women, carriers of each additional copy of SNP rs6584273 in cyclin mediator 1 (CNNM1) had 16% lower T2D risk [OR: 0.84; false discovery rate (FDR)-adjusted P = 0.02]. Among HA women, several variants were significantly associated with T2D risk, including rs10861279 in solute carrier family 41 (anion exchanger), member 2 (SLC41A2) (OR: 0.54; FDR-adjusted P = 0.04), rs7174119 in nonimprinted in Prader-Willi/Angelman syndrome 1 (NIPA1) (OR: 1.27; FDR-adjusted P = 0.04), and 2 SNPs in mitochondrial RNA splicing 2 (MRS2) (rs7738943: OR = 1.55, FDR-adjusted P = 0.01; rs1056285: OR = 1.48, FDR-adjusted P = 0.02). Even with the most conservative Bonferroni adjustment, two 2-SNP-haplotypes in SLC41A2 and MRS2 region were significantly associated with T2D risk (rs12582312-rs10861279: P = 0.0006; rs1056285-rs7738943: P = 0.002). Among women with magnesium intake in the lowest 30% (AA: ≤0.164 g/d; HA: ≤0.185 g/d), 4 SNP signals were strengthened [rs11590362 in claudin 19 (CLDN19), rs823154 in SLC41A1, rs5929706 and rs5930817 in membra; HA: ≥0.313 g/d), rs6584273 in CNNM1 (OR: 0.71; FDR-adjusted P = 0.04) and rs1800467 in potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) (OR: 2.50; FDR-adjusted P = 0.01) were significantly associated with T2D risk.
Our findings suggest important associations between genetic variations in magnesium-related ion channel genes and T2D risk in AA and HA women that vary by amount of magnesium intake.</description><subject>Aged</subject><subject>Biochemical, Molecular, and Genetic Mechanisms</subject><subject>Black or African American - genetics</subject><subject>Body Mass Index</subject><subject>Case-Control Studies</subject><subject>Cation Transport Proteins - genetics</subject><subject>Claudins - genetics</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Dietary Supplements</subject><subject>Female</subject><subject>Genetic Loci</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-Wide Association Study</subject><subject>Genotyping Techniques</subject><subject>Haplotypes</subject><subject>Hispanic or Latino - genetics</subject><subject>Humans</subject><subject>Ion Channels - genetics</subject><subject>Logistic Models</subject><subject>Magnesium - administration & dosage</subject><subject>Magnesium - blood</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Postmenopause</subject><subject>Potassium Channels, Inwardly Rectifying - genetics</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><issn>0022-3166</issn><issn>1541-6100</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1rGzEUFKElcdwcey069rKuvlbWXgompEkh0Evu4q305MjZ1brSOiW3_PSqODXt6T3eDDOPGUI-craSnWq_7NKKc7USTCrTnZEFbxVvNGfsHVkwJkQjudYX5LKUHWOMq86ckwvRrqVUrV6Q11tMOEdHnyFHmOOUCo2JjrBNWOJhbDIOMKOnFaHuEVLCoVT4hUII6GbqI_Q4Y6E5licK45S2dBNydJDoZsTjAsnTu1j2kKrT6fprGjF9IO8DDAWv3uaSPHy7ebi-a-5_3H6_3tw3TrVybkyvje8g6ADAVOCt8L5DkJ5759doQsVZL6FjoTO96gGE8M4xob0JBuWSfD3K7g_9iN5hmjMMdp_jCPnFThDt_0iKj3Y7PVslpW7Fugp8fhPI088DltmOsTgcBkg4HYqtKTPdSlODXZLmSHV5KiVjONlwZv-UZnfJ1tLssbTK__Tvbyf235bkb8vdlyM</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Chan, Kei Hang K</creator><creator>Chacko, Sara A</creator><creator>Song, Yiqing</creator><creator>Cho, Michele</creator><creator>Eaton, Charles B</creator><creator>Wu, Wen-Chih H</creator><creator>Liu, Simin</creator><general>American Society for Nutrition</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150301</creationdate><title>Genetic variations in magnesium-related ion channels may affect diabetes risk among African American and Hispanic American women</title><author>Chan, Kei Hang K ; Chacko, Sara A ; Song, Yiqing ; Cho, Michele ; Eaton, Charles B ; Wu, Wen-Chih H ; Liu, Simin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-8b68d9af6faa04f152dd9ea3d1dcd7e8fb680b3a90f98b4baa22dcc026d8f8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Biochemical, Molecular, and Genetic Mechanisms</topic><topic>Black or African American - genetics</topic><topic>Body Mass Index</topic><topic>Case-Control Studies</topic><topic>Cation Transport Proteins - genetics</topic><topic>Claudins - genetics</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Dietary Supplements</topic><topic>Female</topic><topic>Genetic Loci</topic><topic>Genetic Predisposition to Disease</topic><topic>Genome-Wide Association Study</topic><topic>Genotyping Techniques</topic><topic>Haplotypes</topic><topic>Hispanic or Latino - genetics</topic><topic>Humans</topic><topic>Ion Channels - genetics</topic><topic>Logistic Models</topic><topic>Magnesium - administration & dosage</topic><topic>Magnesium - blood</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Postmenopause</topic><topic>Potassium Channels, Inwardly Rectifying - genetics</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chan, Kei Hang K</creatorcontrib><creatorcontrib>Chacko, Sara A</creatorcontrib><creatorcontrib>Song, Yiqing</creatorcontrib><creatorcontrib>Cho, Michele</creatorcontrib><creatorcontrib>Eaton, Charles B</creatorcontrib><creatorcontrib>Wu, Wen-Chih H</creatorcontrib><creatorcontrib>Liu, Simin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chan, Kei Hang K</au><au>Chacko, Sara A</au><au>Song, Yiqing</au><au>Cho, Michele</au><au>Eaton, Charles B</au><au>Wu, Wen-Chih H</au><au>Liu, Simin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic variations in magnesium-related ion channels may affect diabetes risk among African American and Hispanic American women</atitle><jtitle>The Journal of nutrition</jtitle><addtitle>J Nutr</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>145</volume><issue>3</issue><spage>418</spage><epage>424</epage><pages>418-424</pages><issn>0022-3166</issn><eissn>1541-6100</eissn><abstract>Prospective studies consistently link low magnesium intake to higher type 2 diabetes (T2D) risk.
We examined the association of common genetic variants [single nucleotide polymorphisms (SNPs)] in genes related to magnesium homeostasis with T2D risk and potential interactions with magnesium intake.
Using the Women's Health Initiative-SNP Health Association Resource (WHI-SHARe) study, we identified 17 magnesium-related ion channel genes (583 SNPs) and examined their associations with T2D risk in 7287 African-American (AA; n = 1949 T2D cases) and 3285 Hispanic-American (HA; n = 611 T2D cases) postmenopausal women. We performed both single- and multiple-locus haplotype analyses.
Among AA women, carriers of each additional copy of SNP rs6584273 in cyclin mediator 1 (CNNM1) had 16% lower T2D risk [OR: 0.84; false discovery rate (FDR)-adjusted P = 0.02]. Among HA women, several variants were significantly associated with T2D risk, including rs10861279 in solute carrier family 41 (anion exchanger), member 2 (SLC41A2) (OR: 0.54; FDR-adjusted P = 0.04), rs7174119 in nonimprinted in Prader-Willi/Angelman syndrome 1 (NIPA1) (OR: 1.27; FDR-adjusted P = 0.04), and 2 SNPs in mitochondrial RNA splicing 2 (MRS2) (rs7738943: OR = 1.55, FDR-adjusted P = 0.01; rs1056285: OR = 1.48, FDR-adjusted P = 0.02). Even with the most conservative Bonferroni adjustment, two 2-SNP-haplotypes in SLC41A2 and MRS2 region were significantly associated with T2D risk (rs12582312-rs10861279: P = 0.0006; rs1056285-rs7738943: P = 0.002). Among women with magnesium intake in the lowest 30% (AA: ≤0.164 g/d; HA: ≤0.185 g/d), 4 SNP signals were strengthened [rs11590362 in claudin 19 (CLDN19), rs823154 in SLC41A1, rs5929706 and rs5930817 in membra; HA: ≥0.313 g/d), rs6584273 in CNNM1 (OR: 0.71; FDR-adjusted P = 0.04) and rs1800467 in potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) (OR: 2.50; FDR-adjusted P = 0.01) were significantly associated with T2D risk.
Our findings suggest important associations between genetic variations in magnesium-related ion channel genes and T2D risk in AA and HA women that vary by amount of magnesium intake.</abstract><cop>United States</cop><pub>American Society for Nutrition</pub><pmid>25733456</pmid><doi>10.3945/jn.114.203489</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Biochemical, Molecular, and Genetic Mechanisms Black or African American - genetics Body Mass Index Case-Control Studies Cation Transport Proteins - genetics Claudins - genetics Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - genetics Dietary Supplements Female Genetic Loci Genetic Predisposition to Disease Genome-Wide Association Study Genotyping Techniques Haplotypes Hispanic or Latino - genetics Humans Ion Channels - genetics Logistic Models Magnesium - administration & dosage Magnesium - blood Middle Aged Polymorphism, Single Nucleotide Postmenopause Potassium Channels, Inwardly Rectifying - genetics Prospective Studies Risk Factors |
| title | Genetic variations in magnesium-related ion channels may affect diabetes risk among African American and Hispanic American women |
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