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The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance

Abnormal-glucose tolerance (Abnl-GT) is due to an imbalance between β-cell function and insulin resistance (IR) and is a major risk factor in cardiovascular disease (CVD). In sub-Saharan Africa, β-cell failure is emerging as an important cause of Abnl-GT (Abnl-GT-β-cell-failure). Visceral adipose ti...

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Autores principales: Wentzel, Annemarie, Duhuze Karera, M. Grace, Patterson, Arielle C., Waldman, Zoe C., Schenk, Blayne R., Mabundo, Lilian S., DuBose, Christopher W., Horlyck-Romanovsky, Margrethe F., Sumner, Anne E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9551031/
https://www.ncbi.nlm.nih.gov/pubmed/36216842
http://dx.doi.org/10.1038/s41598-022-19917-8
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author Wentzel, Annemarie
Duhuze Karera, M. Grace
Patterson, Arielle C.
Waldman, Zoe C.
Schenk, Blayne R.
Mabundo, Lilian S.
DuBose, Christopher W.
Horlyck-Romanovsky, Margrethe F.
Sumner, Anne E.
author_facet Wentzel, Annemarie
Duhuze Karera, M. Grace
Patterson, Arielle C.
Waldman, Zoe C.
Schenk, Blayne R.
Mabundo, Lilian S.
DuBose, Christopher W.
Horlyck-Romanovsky, Margrethe F.
Sumner, Anne E.
author_sort Wentzel, Annemarie
collection PubMed
description Abnormal-glucose tolerance (Abnl-GT) is due to an imbalance between β-cell function and insulin resistance (IR) and is a major risk factor in cardiovascular disease (CVD). In sub-Saharan Africa, β-cell failure is emerging as an important cause of Abnl-GT (Abnl-GT-β-cell-failure). Visceral adipose tissue (VAT) volume and hyperlipidemia are major contributors to CVD risk when Abnl-GT is due to IR (Abnl-GT-IR). Yet, the CVD profile associated with Abnl-GT-β-cell failure is unknown. Therefore, our goals in 450 African-born Blacks (Male: 65%; Age: 39 ± 10 years; BMI 28 ± 5 kg/m(2)), living in America were to: (1) determine Abnl-GT prevalence and etiology; (2) assess by Abnl-GT etiology, associations between four understudied subclinical CVD risk factors in Africans: (a) subclinical myocardial damage (high-sensitivity troponin T (hs-cTnT)); (b) neurohormonal regulation (N-terminal pro-Brain-natriuretic peptide (NT-proBNP)); (c) coagulability (fibrinogen); (d) inflammation (high-sensitivity C-reactive protein (hsCRP)), as well as HbA(1c), Cholesterol/HDL ratio and VAT. Glucose tolerance status was determined by the OGTT. IR was defined by the threshold at the lowest quartile for the Matsuda Index (≤ 2.97). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell-failure was defined as Abnl-GT without IR. VAT was assessed by CT-scan. For both the Abnl-GT-β-cell-failure and Abnl-GT-IR groups, four multiple regression models were performed for hs-cTnT; NT-proBNP; fibrinogen and hsCRP, as dependent variables, with the remaining three biomarkers and HbA(1c), Cholesterol/HDL and VAT as independent variables. Abnl-GT occurred in 38% (170/450). In the Abnl-GT group, β-cell failure occurred in 58% (98/170) and IR in 42% (72/170). VAT and Cholesterol/HDL were significantly lower in Abnl-GT-β-cell-failure group vs the Abnl-GT-IR group (both P < 0.001). In the Abnl-GT-β-cell-failure group: significant associations existed between hscTnT, fibrinogen, hs-CRP, and HbA(1c) (all P < 0.05), and none with Cholesterol/HDL or VAT. In Abnl-GT-IR: hs-cTnT, fibrinogen and hsCRP significantly associated with Cholesterol/HDL (all P < 0.05) and NT-proBNP inversely related to fibrinogen, hsCRP, HbA(1c), Cholesterol/HDL, and VAT (all P < 0.05). The subclinical CVD risk profile differed between Abnl-GT-β-cell failure and Abnl-GT-IR. In Abnl-GT-β-cell failure subclinical CVD risk involved subclinical-myocardial damage, hypercoagulability and increased inflammation, but not hyperlipidemia or visceral adiposity. For Abnl-GT-IR, subclinical CVD risk related to subclinical myocardial damage, neurohormonal dysregulation, inflammation associated with hyperlipidemia and visceral adiposity. ClinicalTrials.gov Identifier: NCT00001853.
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spelling pubmed-95510312022-10-12 The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance Wentzel, Annemarie Duhuze Karera, M. Grace Patterson, Arielle C. Waldman, Zoe C. Schenk, Blayne R. Mabundo, Lilian S. DuBose, Christopher W. Horlyck-Romanovsky, Margrethe F. Sumner, Anne E. Sci Rep Article Abnormal-glucose tolerance (Abnl-GT) is due to an imbalance between β-cell function and insulin resistance (IR) and is a major risk factor in cardiovascular disease (CVD). In sub-Saharan Africa, β-cell failure is emerging as an important cause of Abnl-GT (Abnl-GT-β-cell-failure). Visceral adipose tissue (VAT) volume and hyperlipidemia are major contributors to CVD risk when Abnl-GT is due to IR (Abnl-GT-IR). Yet, the CVD profile associated with Abnl-GT-β-cell failure is unknown. Therefore, our goals in 450 African-born Blacks (Male: 65%; Age: 39 ± 10 years; BMI 28 ± 5 kg/m(2)), living in America were to: (1) determine Abnl-GT prevalence and etiology; (2) assess by Abnl-GT etiology, associations between four understudied subclinical CVD risk factors in Africans: (a) subclinical myocardial damage (high-sensitivity troponin T (hs-cTnT)); (b) neurohormonal regulation (N-terminal pro-Brain-natriuretic peptide (NT-proBNP)); (c) coagulability (fibrinogen); (d) inflammation (high-sensitivity C-reactive protein (hsCRP)), as well as HbA(1c), Cholesterol/HDL ratio and VAT. Glucose tolerance status was determined by the OGTT. IR was defined by the threshold at the lowest quartile for the Matsuda Index (≤ 2.97). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell-failure was defined as Abnl-GT without IR. VAT was assessed by CT-scan. For both the Abnl-GT-β-cell-failure and Abnl-GT-IR groups, four multiple regression models were performed for hs-cTnT; NT-proBNP; fibrinogen and hsCRP, as dependent variables, with the remaining three biomarkers and HbA(1c), Cholesterol/HDL and VAT as independent variables. Abnl-GT occurred in 38% (170/450). In the Abnl-GT group, β-cell failure occurred in 58% (98/170) and IR in 42% (72/170). VAT and Cholesterol/HDL were significantly lower in Abnl-GT-β-cell-failure group vs the Abnl-GT-IR group (both P < 0.001). In the Abnl-GT-β-cell-failure group: significant associations existed between hscTnT, fibrinogen, hs-CRP, and HbA(1c) (all P < 0.05), and none with Cholesterol/HDL or VAT. In Abnl-GT-IR: hs-cTnT, fibrinogen and hsCRP significantly associated with Cholesterol/HDL (all P < 0.05) and NT-proBNP inversely related to fibrinogen, hsCRP, HbA(1c), Cholesterol/HDL, and VAT (all P < 0.05). The subclinical CVD risk profile differed between Abnl-GT-β-cell failure and Abnl-GT-IR. In Abnl-GT-β-cell failure subclinical CVD risk involved subclinical-myocardial damage, hypercoagulability and increased inflammation, but not hyperlipidemia or visceral adiposity. For Abnl-GT-IR, subclinical CVD risk related to subclinical myocardial damage, neurohormonal dysregulation, inflammation associated with hyperlipidemia and visceral adiposity. ClinicalTrials.gov Identifier: NCT00001853. Nature Publishing Group UK 2022-10-10 /pmc/articles/PMC9551031/ /pubmed/36216842 http://dx.doi.org/10.1038/s41598-022-19917-8 Text en © This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wentzel, Annemarie
Duhuze Karera, M. Grace
Patterson, Arielle C.
Waldman, Zoe C.
Schenk, Blayne R.
Mabundo, Lilian S.
DuBose, Christopher W.
Horlyck-Romanovsky, Margrethe F.
Sumner, Anne E.
The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title_full The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title_fullStr The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title_full_unstemmed The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title_short The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
title_sort africans in america study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9551031/
https://www.ncbi.nlm.nih.gov/pubmed/36216842
http://dx.doi.org/10.1038/s41598-022-19917-8
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