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Adipokines demonstrate the interacting influence of central obesity with other cardiometabolic risk factors of metabolic syndrome in Hong Kong Chinese adults

Adipokines demonstrate the interacting influence of central obesity with other cardiometabolic risk factors of metabolic syndrome in Hong Kong Chinese adults
Adipokines demonstrate the interacting influence of central obesity with other cardiometabolic risk factors of metabolic syndrome in Hong Kong Chinese adults
Objective Metabolic syndrome (MetS) or prediabetes is a complex disorder that is defined by a clustering of cardiometabolic risk factors, including obesity, hypertriglyceridemia, reduced high-density lipoprotein (HDL) cholesterol, hypertension, and insulin resistance. Among cardiometabolic risk factors, central obesity plays a key role in the development of MetS through alterations in the secretion of adipokines and interacts with other MetS risk factors to unfavorably influence overall cardiometabolic risk. Obesity has grasped epidemic proportions in Asia, which has the highest number of people with diabetes in the world. But, the importance of central obesity in the clustering of all four MetS risk factors or vice versa in predicting severity of MetS has not yet been investigated in Asian population. Therefore, the present study examined the influence of central obesity on circulating levels of adipokines through its interaction with the clustering of cardiometabolic risk factors of MetS including hyperglycemia, hypertriglyceridemia, dyslipidemia and hypertension in Hong Kong Chinese adults. Subjects Blood samples from 83 Hong Kong Chinese adults, who were previously screened for MetS according to the guideline of the United States National Cholesterol Education Program Expert Panel Adult Treatment Panel III criteria were selected. Insulin and adipokines, including visfatin, chemerin, plasminogen activator inhibitor-1 (PAI-1), resistin, C-C motif chemokine ligand 2 (CCL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), tumour necrosis factor-α (TNF-α), leptin and adiponectin were assessed. Results The interacting effect of central obesity with all of the other four MetS risk factors increased the proinflammatory status of adipokines (TNF-α, leptin) and decreased the anti-inflammatory status of adipokine (adiponectin). Conclusion Our results indicate that the inflammatory status of MetS may be more severe in the presence of central obesity. Adipokines, as biomarkers for pathophysiological changes, may help to improve early patient identification and to predict MetS-associated morbidity and mortality.
1932-6203
Supriya, Rashmi
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Tam, Bjorn T.
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Yu, Angus P.
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Lee, Paul H.
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Lai, Christopher W.
83f3d235-4de6-4462-b3d9-22c377e86afd
Cheng, Kenneth K.
ade5a521-9b33-4448-9fb0-3bddb29ed7e6
Yau, Sonata Y.
de580572-bd73-4081-9c15-37b3dad7f8f7
Chan, Lawrence W.
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Yung, Benjamin Y.
b464af44-b822-4d67-a30d-b13212051dda
Sheridan, Sinead
b4895635-84b8-44b3-977f-ead7a1fb9239
Siu, Parco M.
3a92bd40-810f-44e8-80d3-585b634d0bf6
et al.
Supriya, Rashmi
9c8deec3-9aef-4cc7-97fb-b488e1c61888
Tam, Bjorn T.
d48d482e-0316-49ec-bfd2-d46e48789e7e
Yu, Angus P.
e9174c18-c499-460e-922f-eef235c51319
Lee, Paul H.
02620eab-ae7f-4a1c-bad1-8a50e7e48951
Lai, Christopher W.
83f3d235-4de6-4462-b3d9-22c377e86afd
Cheng, Kenneth K.
ade5a521-9b33-4448-9fb0-3bddb29ed7e6
Yau, Sonata Y.
de580572-bd73-4081-9c15-37b3dad7f8f7
Chan, Lawrence W.
25800c84-e0b6-4193-8623-73d670e0a38e
Yung, Benjamin Y.
b464af44-b822-4d67-a30d-b13212051dda
Sheridan, Sinead
b4895635-84b8-44b3-977f-ead7a1fb9239
Siu, Parco M.
3a92bd40-810f-44e8-80d3-585b634d0bf6

Supriya, Rashmi, Tam, Bjorn T., Yu, Angus P., Lee, Paul H. and Siu, Parco M. , et al. (2018) Adipokines demonstrate the interacting influence of central obesity with other cardiometabolic risk factors of metabolic syndrome in Hong Kong Chinese adults. PLoS ONE, 13 (8), [e0201585]. (doi:10.1371/journal.pone.0201585).

Record type: Article

Abstract

Objective Metabolic syndrome (MetS) or prediabetes is a complex disorder that is defined by a clustering of cardiometabolic risk factors, including obesity, hypertriglyceridemia, reduced high-density lipoprotein (HDL) cholesterol, hypertension, and insulin resistance. Among cardiometabolic risk factors, central obesity plays a key role in the development of MetS through alterations in the secretion of adipokines and interacts with other MetS risk factors to unfavorably influence overall cardiometabolic risk. Obesity has grasped epidemic proportions in Asia, which has the highest number of people with diabetes in the world. But, the importance of central obesity in the clustering of all four MetS risk factors or vice versa in predicting severity of MetS has not yet been investigated in Asian population. Therefore, the present study examined the influence of central obesity on circulating levels of adipokines through its interaction with the clustering of cardiometabolic risk factors of MetS including hyperglycemia, hypertriglyceridemia, dyslipidemia and hypertension in Hong Kong Chinese adults. Subjects Blood samples from 83 Hong Kong Chinese adults, who were previously screened for MetS according to the guideline of the United States National Cholesterol Education Program Expert Panel Adult Treatment Panel III criteria were selected. Insulin and adipokines, including visfatin, chemerin, plasminogen activator inhibitor-1 (PAI-1), resistin, C-C motif chemokine ligand 2 (CCL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), tumour necrosis factor-α (TNF-α), leptin and adiponectin were assessed. Results The interacting effect of central obesity with all of the other four MetS risk factors increased the proinflammatory status of adipokines (TNF-α, leptin) and decreased the anti-inflammatory status of adipokine (adiponectin). Conclusion Our results indicate that the inflammatory status of MetS may be more severe in the presence of central obesity. Adipokines, as biomarkers for pathophysiological changes, may help to improve early patient identification and to predict MetS-associated morbidity and mortality.

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More information

Accepted/In Press date: 18 July 2018
Published date: 16 August 2018
Additional Information: Funding Information: We declare all the funding or sources of support received during this specific study as the following, and all the funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This study was supported by the Hong Kong Research Grants Council Hong Kong Ph.D. Fellowship Scheme (RTVX PF13-11753), the Hong Kong Polytechnic University Research Fund (RTAS and 1-ZE17), The University of Hong Kong Seed Fund for Basic Research, and the Hong Kong Research Grants Council General Research Fund (PolyU 5632/10M). Publisher Copyright: © 2018 Supriya et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Local EPrints ID: 475098
URI: http://eprints.soton.ac.uk/id/eprint/475098
ISSN: 1932-6203
PURE UUID: 09c0f1f7-71a6-4106-a0bd-698da711642a
ORCID for Paul H. Lee: ORCID iD orcid.org/0000-0002-5729-6450

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Date deposited: 09 Mar 2023 19:08
Last modified: 18 Mar 2024 04:09

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Contributors

Author: Rashmi Supriya
Author: Bjorn T. Tam
Author: Angus P. Yu
Author: Paul H. Lee ORCID iD
Author: Christopher W. Lai
Author: Kenneth K. Cheng
Author: Sonata Y. Yau
Author: Lawrence W. Chan
Author: Benjamin Y. Yung
Author: Sinead Sheridan
Author: Parco M. Siu
Corporate Author: et al.

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