Adipokines and subclinical cardiovascular disease in post-menopausal women: Study of women’s health across the nation

Susan A. Everson-Rose; Emma J.M. Barinas-Mitchell; Samar R. El Khoudary; Hsin Hui Huang; Qi Wang; Imke Janssen; Rebecca C. Thurston; Elizabeth A. Jackson; Melissa E. Lewis; Carrie Karvonen-Gutierrez; Peter Mancuso; Carol A. Derby

doi:10.1161/JAHA.120.019173

Adipokines and subclinical cardiovascular disease in post-menopausal women: Study of women’s health across the nation

Susan A. Everson-Rose, Emma J.M. Barinas-Mitchell, Samar R. El Khoudary, Hsin Hui Huang, Qi Wang, Imke Janssen, Rebecca C. Thurston, Elizabeth A. Jackson, Melissa E. Lewis, Carrie Karvonen-Gutierrez, Peter Mancuso, Carol A. Derby

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

BACKGROUND: The menopausal transition is characterized by increased cardiovascular risk, weight gain, and increased adipos-ity for many women. The adipose-derived secretory proteins adiponectin and leptin are associated with insulin resistance, metabolic syndrome, and cardiovascular disease but their role in subclinical atherosclerotic disease is unclear. This cross-sectional study evaluated the associations of adiponectin and leptin with carotid artery intima-media thickness, adventitial diameter, presence of carotid plaques, and brachial-ankle pulse wave velocity (baPWV) in women aged 54 to 65 years. METHODS AND RESULTS: Participants were 1399 women from SWAN (Study of Women’s Health Across the Nation), a community-based study of women transitioning through menopause. Carotid ultrasound and baPWV measures were obtained at SWAN follow-up visits 12 or 13, when 97% of participants were post-menopausal. Adipokines were assayed from serum speci-mens obtained concurrently at these visits. Linear and logistic regression models were used to evaluate adiponectin or leptin, both log-transformed attributable to skewness, in relationship to carotid artery intima-media thickness, adventitial diameter, baPWV, and presence of carotid plaque. Covariates included age, race, study site, smoking, alcohol use, obesity, cardiovascular disease risk factors, and menopausal status. Lower levels of adiponectin were related to greater carotid artery intima-media thickness, wider adventitial diameter, and faster baPWV; associations were attenuated after adjusting for cardiovascular disease risk factors. Higher levels of leptin were associated with greater carotid artery intima-media thickness and wider adventitial diameter in minimally and fully adjusted models, and contrary to expectation, with slower baPWV, particularly among women with diabetes mellitus or obesity. CONCLUSIONS: Adiponectin and leptin are 2 important inflammatory pathways that may contribute to adverse subclinical cardiovascular disease risk profiles in women at midlife.

Original language	English (US)
Article number	e019173
Journal	Journal of the American Heart Association
Volume	10
Issue number	7
DOIs	https://doi.org/10.1161/JAHA.120.019173
State	Published - 2021

Bibliographical note

Funding Information:
The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women?s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women?s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication.

Funding Information:
The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women’s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women’s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication.

Publisher Copyright:
© 2021 The Authors.

Keywords

Adiponectin
Atherosclerosis
Cardiovascular risk factors
Leptin
Menopause

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1161/JAHA.120.019173

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Everson-Rose, S. A., Barinas-Mitchell, E. J. M., El Khoudary, S. R., Huang, H. H., Wang, Q., Janssen, I., Thurston, R. C., Jackson, E. A., Lewis, M. E., Karvonen-Gutierrez, C., Mancuso, P., & Derby, C. A. (2021). Adipokines and subclinical cardiovascular disease in post-menopausal women: Study of women’s health across the nation. Journal of the American Heart Association, 10(7), Article e019173. https://doi.org/10.1161/JAHA.120.019173

Everson-Rose, SA, Barinas-Mitchell, EJM, El Khoudary, SR, Huang, HH, Wang, Q, Janssen, I, Thurston, RC, Jackson, EA, Lewis, ME, Karvonen-Gutierrez, C, Mancuso, P & Derby, CA 2021, 'Adipokines and subclinical cardiovascular disease in post-menopausal women: Study of women’s health across the nation', Journal of the American Heart Association, vol. 10, no. 7, e019173. https://doi.org/10.1161/JAHA.120.019173

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abstract = "BACKGROUND: The menopausal transition is characterized by increased cardiovascular risk, weight gain, and increased adipos-ity for many women. The adipose-derived secretory proteins adiponectin and leptin are associated with insulin resistance, metabolic syndrome, and cardiovascular disease but their role in subclinical atherosclerotic disease is unclear. This cross-sectional study evaluated the associations of adiponectin and leptin with carotid artery intima-media thickness, adventitial diameter, presence of carotid plaques, and brachial-ankle pulse wave velocity (baPWV) in women aged 54 to 65 years. METHODS AND RESULTS: Participants were 1399 women from SWAN (Study of Women{\textquoteright}s Health Across the Nation), a community-based study of women transitioning through menopause. Carotid ultrasound and baPWV measures were obtained at SWAN follow-up visits 12 or 13, when 97% of participants were post-menopausal. Adipokines were assayed from serum speci-mens obtained concurrently at these visits. Linear and logistic regression models were used to evaluate adiponectin or leptin, both log-transformed attributable to skewness, in relationship to carotid artery intima-media thickness, adventitial diameter, baPWV, and presence of carotid plaque. Covariates included age, race, study site, smoking, alcohol use, obesity, cardiovascular disease risk factors, and menopausal status. Lower levels of adiponectin were related to greater carotid artery intima-media thickness, wider adventitial diameter, and faster baPWV; associations were attenuated after adjusting for cardiovascular disease risk factors. Higher levels of leptin were associated with greater carotid artery intima-media thickness and wider adventitial diameter in minimally and fully adjusted models, and contrary to expectation, with slower baPWV, particularly among women with diabetes mellitus or obesity. CONCLUSIONS: Adiponectin and leptin are 2 important inflammatory pathways that may contribute to adverse subclinical cardiovascular disease risk profiles in women at midlife.",

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author = "Everson-Rose, {Susan A.} and Barinas-Mitchell, {Emma J.M.} and {El Khoudary}, {Samar R.} and Huang, {Hsin Hui} and Qi Wang and Imke Janssen and Thurston, {Rebecca C.} and Jackson, {Elizabeth A.} and Lewis, {Melissa E.} and Carrie Karvonen-Gutierrez and Peter Mancuso and Derby, {Carol A.}",

note = "Funding Information: The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women?s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women?s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication. Funding Information: The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women{\textquoteright}s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women{\textquoteright}s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication. Publisher Copyright: {\textcopyright} 2021 The Authors.",

year = "2021",

doi = "10.1161/JAHA.120.019173",

language = "English (US)",

volume = "10",

journal = "Journal of the American Heart Association",

issn = "2047-9980",

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TY - JOUR

T1 - Adipokines and subclinical cardiovascular disease in post-menopausal women

T2 - Study of women’s health across the nation

AU - Everson-Rose, Susan A.

AU - Barinas-Mitchell, Emma J.M.

AU - El Khoudary, Samar R.

AU - Huang, Hsin Hui

AU - Wang, Qi

AU - Janssen, Imke

AU - Thurston, Rebecca C.

AU - Jackson, Elizabeth A.

AU - Lewis, Melissa E.

AU - Karvonen-Gutierrez, Carrie

AU - Mancuso, Peter

AU - Derby, Carol A.

N1 - Funding Information: The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women?s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women?s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication. Funding Information: The SWAN study has grant support from the National Institutes of Health, Department of Health and Human Services (DHHS), through the National Institute on Aging, the National Institute of Nursing Research and the National Institutes of Health Office of Research on Women’s Health (Grants U01NR004061; U01AG012505, U01AG012535, U01AG012531, U01AG012539, U01AG012546, U01AG012553, U01AG012554, U01AG012495). The Chicago site of SWAN also is supported by the Charles J. and Margaret Roberts Trust. This publication also was supported in part by the National Center for Research Resources and the National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through University of California San Francisco (UCSF)-Clinical and Translational Science Institute (CTSI) Grant Number UL1 RR024131 and UMN-CTSI Grant Number UL1 TR002494, and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. The contents of this article are solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, National Institute of Nursing Research, Office of Research on Women’s Health, National Center for Research Resources, NCATS, or the National Institutes of Health. None of the funders had any involvement in the study design, the collection, analysis, and interpretation of data, in writing this article, or in the decision to submit this article for publication. Publisher Copyright: © 2021 The Authors.

PY - 2021

Y1 - 2021

N2 - BACKGROUND: The menopausal transition is characterized by increased cardiovascular risk, weight gain, and increased adipos-ity for many women. The adipose-derived secretory proteins adiponectin and leptin are associated with insulin resistance, metabolic syndrome, and cardiovascular disease but their role in subclinical atherosclerotic disease is unclear. This cross-sectional study evaluated the associations of adiponectin and leptin with carotid artery intima-media thickness, adventitial diameter, presence of carotid plaques, and brachial-ankle pulse wave velocity (baPWV) in women aged 54 to 65 years. METHODS AND RESULTS: Participants were 1399 women from SWAN (Study of Women’s Health Across the Nation), a community-based study of women transitioning through menopause. Carotid ultrasound and baPWV measures were obtained at SWAN follow-up visits 12 or 13, when 97% of participants were post-menopausal. Adipokines were assayed from serum speci-mens obtained concurrently at these visits. Linear and logistic regression models were used to evaluate adiponectin or leptin, both log-transformed attributable to skewness, in relationship to carotid artery intima-media thickness, adventitial diameter, baPWV, and presence of carotid plaque. Covariates included age, race, study site, smoking, alcohol use, obesity, cardiovascular disease risk factors, and menopausal status. Lower levels of adiponectin were related to greater carotid artery intima-media thickness, wider adventitial diameter, and faster baPWV; associations were attenuated after adjusting for cardiovascular disease risk factors. Higher levels of leptin were associated with greater carotid artery intima-media thickness and wider adventitial diameter in minimally and fully adjusted models, and contrary to expectation, with slower baPWV, particularly among women with diabetes mellitus or obesity. CONCLUSIONS: Adiponectin and leptin are 2 important inflammatory pathways that may contribute to adverse subclinical cardiovascular disease risk profiles in women at midlife.

AB - BACKGROUND: The menopausal transition is characterized by increased cardiovascular risk, weight gain, and increased adipos-ity for many women. The adipose-derived secretory proteins adiponectin and leptin are associated with insulin resistance, metabolic syndrome, and cardiovascular disease but their role in subclinical atherosclerotic disease is unclear. This cross-sectional study evaluated the associations of adiponectin and leptin with carotid artery intima-media thickness, adventitial diameter, presence of carotid plaques, and brachial-ankle pulse wave velocity (baPWV) in women aged 54 to 65 years. METHODS AND RESULTS: Participants were 1399 women from SWAN (Study of Women’s Health Across the Nation), a community-based study of women transitioning through menopause. Carotid ultrasound and baPWV measures were obtained at SWAN follow-up visits 12 or 13, when 97% of participants were post-menopausal. Adipokines were assayed from serum speci-mens obtained concurrently at these visits. Linear and logistic regression models were used to evaluate adiponectin or leptin, both log-transformed attributable to skewness, in relationship to carotid artery intima-media thickness, adventitial diameter, baPWV, and presence of carotid plaque. Covariates included age, race, study site, smoking, alcohol use, obesity, cardiovascular disease risk factors, and menopausal status. Lower levels of adiponectin were related to greater carotid artery intima-media thickness, wider adventitial diameter, and faster baPWV; associations were attenuated after adjusting for cardiovascular disease risk factors. Higher levels of leptin were associated with greater carotid artery intima-media thickness and wider adventitial diameter in minimally and fully adjusted models, and contrary to expectation, with slower baPWV, particularly among women with diabetes mellitus or obesity. CONCLUSIONS: Adiponectin and leptin are 2 important inflammatory pathways that may contribute to adverse subclinical cardiovascular disease risk profiles in women at midlife.

KW - Adiponectin

KW - Atherosclerosis

KW - Cardiovascular risk factors

KW - Leptin

KW - Menopause

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DO - 10.1161/JAHA.120.019173

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JO - Journal of the American Heart Association

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ER -

Adipokines and subclinical cardiovascular disease in post-menopausal women: Study of women’s health across the nation

Abstract

Bibliographical note

Keywords

UN SDGs

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