1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure
Abnormal glucose tolerance (Abnl-GT) is due to an imbalance between insulin resistance (IR) and β-cell function. Recent data from Africa suggest that β-cell failure contributes to the development of Abnl-GT more than previously recognized. Therefore in 490 African-born Blacks living in the United St...
Gespeichert in:
Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2021-06, Vol.70 (Supplement_1) |
---|---|
Hauptverfasser: | , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | |
---|---|
container_issue | Supplement_1 |
container_start_page | |
container_title | Diabetes (New York, N.Y.) |
container_volume | 70 |
creator | ISHIMWE, MARIE CONSOLATRICE SAGE HORMENU, THOMAS SHOUP, ELYSSA M. OSEI-TUTU, NANA H. PATTERSON, ARIELLE WENTZEL, ANNEMARIE BAGHERI, MOHAMMAD-HADI DUBOSE, CHRISTOPHER MABUNDO, LILIAN HA, JOON SHERMAN, ARTHUR SUMNER, ANNE E. |
description | Abnormal glucose tolerance (Abnl-GT) is due to an imbalance between insulin resistance (IR) and β-cell function. Recent data from Africa suggest that β-cell failure contributes to the development of Abnl-GT more than previously recognized. Therefore in 490 African-born Blacks living in the United States (Male 64%, Age 38±10y (mean±SD), we compared the prevalence and metabolic characteristics of Abnl-GT due to IR (Abnl-GT-IR) to Abnl-GT due to β-cell-failure (Abnl-GT-β-cell-failure). Based on OGTT, Abnl-GT was defined as fasting glucose≥100 mg/dL or 2h glucose≥140 mg/dL. Visceral adipose tissue (VAT), triglyceride (TG) and 10y-Cardiovascular Risk-Score (CVD-Risk-Score) were measured. The cohort was divided into quartiles of HOMA-IR and quartiles of Matsuda Index. IR was defined by thresholds at the upper quartile of HOMA-IR (≥2.05) or the lowest quartile of the Matsuda index (≤2.97). Diagnosis of Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell failure was defined as Abnl-GT without IR. Abnl-GT occurred in 38% (181/490) of Africans. Of the Africans with Abnl-GT, insulin resistance occurred in 38% (68/181) and β-cell-failure occurred in 62% (113/181) of the Africans. Compared to Africans with Abnl-GT-β-cell-failure, Africans with Abnl-GT-IR had higher BMI (31.0±4.5 vs. 27.4±3.8 kg/m2), VAT (160±72 vs. 111±65 cm2), TG (106±52 vs. 77±39 mg/dL) (all P |
doi_str_mv | 10.2337/db21-1089-P |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2562265727</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2562265727</sourcerecordid><originalsourceid>FETCH-LOGICAL-c647-1f111812d7e58e79a0f76b9617556a43fc3e73f0bb9e14ca5dbf3e7eef41cd0e3</originalsourceid><addsrcrecordid>eNotkM1KAzEQgIMoWKsnXyDgUVLzs5t0eytrWwsFi_TgLWR3J7IlTWrSFfo0Powv5tbKHGYYvvnhQ-ie0REXQj01FWeE0XFB1hdowApREMHV-yUaUMo4YapQ1-gmpS2lVPYxQNszPcHTyoe4Mw4vXFeHBHgTHETja8Bl8Ak-O-jrhJ9hD77BwePZoQ0ufBwneOlT51qP3yC16fA385VG-OeblOAcnpvWdRFu0ZU1LsHdfx6izXy2KV_I6nWxLKcrUstMEWYZY2PGGwX5GFRhqFWyKiRTeS5NJmwtQAlLq6oAltUmbyrbdwBsxuqGghiih_PafQz90-mgt6GLvr-oeS45l7niqqcez1QdQ0oRrN7HdmfiUTOqTy71yaU-2dFr8QuxXGcZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2562265727</pqid></control><display><type>article</type><title>1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>ISHIMWE, MARIE CONSOLATRICE SAGE ; HORMENU, THOMAS ; SHOUP, ELYSSA M. ; OSEI-TUTU, NANA H. ; PATTERSON, ARIELLE ; WENTZEL, ANNEMARIE ; BAGHERI, MOHAMMAD-HADI ; DUBOSE, CHRISTOPHER ; MABUNDO, LILIAN ; HA, JOON ; SHERMAN, ARTHUR ; SUMNER, ANNE E.</creator><creatorcontrib>ISHIMWE, MARIE CONSOLATRICE SAGE ; HORMENU, THOMAS ; SHOUP, ELYSSA M. ; OSEI-TUTU, NANA H. ; PATTERSON, ARIELLE ; WENTZEL, ANNEMARIE ; BAGHERI, MOHAMMAD-HADI ; DUBOSE, CHRISTOPHER ; MABUNDO, LILIAN ; HA, JOON ; SHERMAN, ARTHUR ; SUMNER, ANNE E.</creatorcontrib><description>Abnormal glucose tolerance (Abnl-GT) is due to an imbalance between insulin resistance (IR) and β-cell function. Recent data from Africa suggest that β-cell failure contributes to the development of Abnl-GT more than previously recognized. Therefore in 490 African-born Blacks living in the United States (Male 64%, Age 38±10y (mean±SD), we compared the prevalence and metabolic characteristics of Abnl-GT due to IR (Abnl-GT-IR) to Abnl-GT due to β-cell-failure (Abnl-GT-β-cell-failure). Based on OGTT, Abnl-GT was defined as fasting glucose≥100 mg/dL or 2h glucose≥140 mg/dL. Visceral adipose tissue (VAT), triglyceride (TG) and 10y-Cardiovascular Risk-Score (CVD-Risk-Score) were measured. The cohort was divided into quartiles of HOMA-IR and quartiles of Matsuda Index. IR was defined by thresholds at the upper quartile of HOMA-IR (≥2.05) or the lowest quartile of the Matsuda index (≤2.97). Diagnosis of Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell failure was defined as Abnl-GT without IR. Abnl-GT occurred in 38% (181/490) of Africans. Of the Africans with Abnl-GT, insulin resistance occurred in 38% (68/181) and β-cell-failure occurred in 62% (113/181) of the Africans. Compared to Africans with Abnl-GT-β-cell-failure, Africans with Abnl-GT-IR had higher BMI (31.0±4.5 vs. 27.4±3.8 kg/m2), VAT (160±72 vs. 111±65 cm2), TG (106±52 vs. 77±39 mg/dL) (all P<0.001) and CVD-Risk-Score (26±24 vs. 19±17) (P<0.05). Independent of whether IR was defined by HOMA-IR or Matsuda index, results were similar. Alcohol intake was higher in the Abnl-GT-IR group (P=0.05), but other potential confounders such as years in the United States, income, education, sedentary behavior and fiber intake did not differ. Overall, Abnl-GT-IR was less common than Abnl-GT-β-cell-failure, but the metabolic profile was worse in Abnl-GT-IR. To determine the clinical course for these two types of Abnl-GT, prospective study design needs to include methodology to both diagnose Abnl-GT and elucidate the cause.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db21-1089-P</identifier><language>eng</language><publisher>New York: American Diabetes Association</publisher><subject>Adipose tissue ; Beta cells ; Cardiovascular diseases ; Diabetes ; Etiology ; Glucose ; Glucose tolerance ; Insulin ; Insulin resistance ; Metabolism</subject><ispartof>Diabetes (New York, N.Y.), 2021-06, Vol.70 (Supplement_1)</ispartof><rights>Copyright American Diabetes Association Jun 1, 2021</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>314,777,781,27905,27906</link.rule.ids></links><search><creatorcontrib>ISHIMWE, MARIE CONSOLATRICE SAGE</creatorcontrib><creatorcontrib>HORMENU, THOMAS</creatorcontrib><creatorcontrib>SHOUP, ELYSSA M.</creatorcontrib><creatorcontrib>OSEI-TUTU, NANA H.</creatorcontrib><creatorcontrib>PATTERSON, ARIELLE</creatorcontrib><creatorcontrib>WENTZEL, ANNEMARIE</creatorcontrib><creatorcontrib>BAGHERI, MOHAMMAD-HADI</creatorcontrib><creatorcontrib>DUBOSE, CHRISTOPHER</creatorcontrib><creatorcontrib>MABUNDO, LILIAN</creatorcontrib><creatorcontrib>HA, JOON</creatorcontrib><creatorcontrib>SHERMAN, ARTHUR</creatorcontrib><creatorcontrib>SUMNER, ANNE E.</creatorcontrib><title>1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure</title><title>Diabetes (New York, N.Y.)</title><description>Abnormal glucose tolerance (Abnl-GT) is due to an imbalance between insulin resistance (IR) and β-cell function. Recent data from Africa suggest that β-cell failure contributes to the development of Abnl-GT more than previously recognized. Therefore in 490 African-born Blacks living in the United States (Male 64%, Age 38±10y (mean±SD), we compared the prevalence and metabolic characteristics of Abnl-GT due to IR (Abnl-GT-IR) to Abnl-GT due to β-cell-failure (Abnl-GT-β-cell-failure). Based on OGTT, Abnl-GT was defined as fasting glucose≥100 mg/dL or 2h glucose≥140 mg/dL. Visceral adipose tissue (VAT), triglyceride (TG) and 10y-Cardiovascular Risk-Score (CVD-Risk-Score) were measured. The cohort was divided into quartiles of HOMA-IR and quartiles of Matsuda Index. IR was defined by thresholds at the upper quartile of HOMA-IR (≥2.05) or the lowest quartile of the Matsuda index (≤2.97). Diagnosis of Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell failure was defined as Abnl-GT without IR. Abnl-GT occurred in 38% (181/490) of Africans. Of the Africans with Abnl-GT, insulin resistance occurred in 38% (68/181) and β-cell-failure occurred in 62% (113/181) of the Africans. Compared to Africans with Abnl-GT-β-cell-failure, Africans with Abnl-GT-IR had higher BMI (31.0±4.5 vs. 27.4±3.8 kg/m2), VAT (160±72 vs. 111±65 cm2), TG (106±52 vs. 77±39 mg/dL) (all P<0.001) and CVD-Risk-Score (26±24 vs. 19±17) (P<0.05). Independent of whether IR was defined by HOMA-IR or Matsuda index, results were similar. Alcohol intake was higher in the Abnl-GT-IR group (P=0.05), but other potential confounders such as years in the United States, income, education, sedentary behavior and fiber intake did not differ. Overall, Abnl-GT-IR was less common than Abnl-GT-β-cell-failure, but the metabolic profile was worse in Abnl-GT-IR. To determine the clinical course for these two types of Abnl-GT, prospective study design needs to include methodology to both diagnose Abnl-GT and elucidate the cause.</description><subject>Adipose tissue</subject><subject>Beta cells</subject><subject>Cardiovascular diseases</subject><subject>Diabetes</subject><subject>Etiology</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Metabolism</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNotkM1KAzEQgIMoWKsnXyDgUVLzs5t0eytrWwsFi_TgLWR3J7IlTWrSFfo0Powv5tbKHGYYvvnhQ-ie0REXQj01FWeE0XFB1hdowApREMHV-yUaUMo4YapQ1-gmpS2lVPYxQNszPcHTyoe4Mw4vXFeHBHgTHETja8Bl8Ak-O-jrhJ9hD77BwePZoQ0ufBwneOlT51qP3yC16fA385VG-OeblOAcnpvWdRFu0ZU1LsHdfx6izXy2KV_I6nWxLKcrUstMEWYZY2PGGwX5GFRhqFWyKiRTeS5NJmwtQAlLq6oAltUmbyrbdwBsxuqGghiih_PafQz90-mgt6GLvr-oeS45l7niqqcez1QdQ0oRrN7HdmfiUTOqTy71yaU-2dFr8QuxXGcZ</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>ISHIMWE, MARIE CONSOLATRICE SAGE</creator><creator>HORMENU, THOMAS</creator><creator>SHOUP, ELYSSA M.</creator><creator>OSEI-TUTU, NANA H.</creator><creator>PATTERSON, ARIELLE</creator><creator>WENTZEL, ANNEMARIE</creator><creator>BAGHERI, MOHAMMAD-HADI</creator><creator>DUBOSE, CHRISTOPHER</creator><creator>MABUNDO, LILIAN</creator><creator>HA, JOON</creator><creator>SHERMAN, ARTHUR</creator><creator>SUMNER, ANNE E.</creator><general>American Diabetes Association</general><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20210601</creationdate><title>1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure</title><author>ISHIMWE, MARIE CONSOLATRICE SAGE ; HORMENU, THOMAS ; SHOUP, ELYSSA M. ; OSEI-TUTU, NANA H. ; PATTERSON, ARIELLE ; WENTZEL, ANNEMARIE ; BAGHERI, MOHAMMAD-HADI ; DUBOSE, CHRISTOPHER ; MABUNDO, LILIAN ; HA, JOON ; SHERMAN, ARTHUR ; SUMNER, ANNE E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c647-1f111812d7e58e79a0f76b9617556a43fc3e73f0bb9e14ca5dbf3e7eef41cd0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adipose tissue</topic><topic>Beta cells</topic><topic>Cardiovascular diseases</topic><topic>Diabetes</topic><topic>Etiology</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ISHIMWE, MARIE CONSOLATRICE SAGE</creatorcontrib><creatorcontrib>HORMENU, THOMAS</creatorcontrib><creatorcontrib>SHOUP, ELYSSA M.</creatorcontrib><creatorcontrib>OSEI-TUTU, NANA H.</creatorcontrib><creatorcontrib>PATTERSON, ARIELLE</creatorcontrib><creatorcontrib>WENTZEL, ANNEMARIE</creatorcontrib><creatorcontrib>BAGHERI, MOHAMMAD-HADI</creatorcontrib><creatorcontrib>DUBOSE, CHRISTOPHER</creatorcontrib><creatorcontrib>MABUNDO, LILIAN</creatorcontrib><creatorcontrib>HA, JOON</creatorcontrib><creatorcontrib>SHERMAN, ARTHUR</creatorcontrib><creatorcontrib>SUMNER, ANNE E.</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>ISHIMWE, MARIE CONSOLATRICE SAGE</au><au>HORMENU, THOMAS</au><au>SHOUP, ELYSSA M.</au><au>OSEI-TUTU, NANA H.</au><au>PATTERSON, ARIELLE</au><au>WENTZEL, ANNEMARIE</au><au>BAGHERI, MOHAMMAD-HADI</au><au>DUBOSE, CHRISTOPHER</au><au>MABUNDO, LILIAN</au><au>HA, JOON</au><au>SHERMAN, ARTHUR</au><au>SUMNER, ANNE E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><date>2021-06-01</date><risdate>2021</risdate><volume>70</volume><issue>Supplement_1</issue><issn>0012-1797</issn><eissn>1939-327X</eissn><abstract>Abnormal glucose tolerance (Abnl-GT) is due to an imbalance between insulin resistance (IR) and β-cell function. Recent data from Africa suggest that β-cell failure contributes to the development of Abnl-GT more than previously recognized. Therefore in 490 African-born Blacks living in the United States (Male 64%, Age 38±10y (mean±SD), we compared the prevalence and metabolic characteristics of Abnl-GT due to IR (Abnl-GT-IR) to Abnl-GT due to β-cell-failure (Abnl-GT-β-cell-failure). Based on OGTT, Abnl-GT was defined as fasting glucose≥100 mg/dL or 2h glucose≥140 mg/dL. Visceral adipose tissue (VAT), triglyceride (TG) and 10y-Cardiovascular Risk-Score (CVD-Risk-Score) were measured. The cohort was divided into quartiles of HOMA-IR and quartiles of Matsuda Index. IR was defined by thresholds at the upper quartile of HOMA-IR (≥2.05) or the lowest quartile of the Matsuda index (≤2.97). Diagnosis of Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell failure was defined as Abnl-GT without IR. Abnl-GT occurred in 38% (181/490) of Africans. Of the Africans with Abnl-GT, insulin resistance occurred in 38% (68/181) and β-cell-failure occurred in 62% (113/181) of the Africans. Compared to Africans with Abnl-GT-β-cell-failure, Africans with Abnl-GT-IR had higher BMI (31.0±4.5 vs. 27.4±3.8 kg/m2), VAT (160±72 vs. 111±65 cm2), TG (106±52 vs. 77±39 mg/dL) (all P<0.001) and CVD-Risk-Score (26±24 vs. 19±17) (P<0.05). Independent of whether IR was defined by HOMA-IR or Matsuda index, results were similar. Alcohol intake was higher in the Abnl-GT-IR group (P=0.05), but other potential confounders such as years in the United States, income, education, sedentary behavior and fiber intake did not differ. Overall, Abnl-GT-IR was less common than Abnl-GT-β-cell-failure, but the metabolic profile was worse in Abnl-GT-IR. To determine the clinical course for these two types of Abnl-GT, prospective study design needs to include methodology to both diagnose Abnl-GT and elucidate the cause.</abstract><cop>New York</cop><pub>American Diabetes Association</pub><doi>10.2337/db21-1089-P</doi></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0012-1797 |
ispartof | Diabetes (New York, N.Y.), 2021-06, Vol.70 (Supplement_1) |
issn | 0012-1797 1939-327X |
language | eng |
recordid | cdi_proquest_journals_2562265727 |
source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
subjects | Adipose tissue Beta cells Cardiovascular diseases Diabetes Etiology Glucose Glucose tolerance Insulin Insulin resistance Metabolism |
title | 1089-P: Abnormal Glucose Tolerance Consequences Depend on Etiology: Insulin Resistance vs. ß-Cell Failure |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T03%3A36%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=1089-P:%20Abnormal%20Glucose%20Tolerance%20Consequences%20Depend%20on%20Etiology:%20Insulin%20Resistance%20vs.%20%C3%9F-Cell%20Failure&rft.jtitle=Diabetes%20(New%20York,%20N.Y.)&rft.au=ISHIMWE,%20MARIE%20CONSOLATRICE%20SAGE&rft.date=2021-06-01&rft.volume=70&rft.issue=Supplement_1&rft.issn=0012-1797&rft.eissn=1939-327X&rft_id=info:doi/10.2337/db21-1089-P&rft_dat=%3Cproquest_cross%3E2562265727%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2562265727&rft_id=info:pmid/&rfr_iscdi=true |