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Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals
Cardiotrophin-1 is known to be a key regulator of energy homeostasis, as well as glucose and lipid metabolism in vivo. However, there are inconsistent results of the association between cardiotrophin-1 and obesity in humans, possibly confounded by hyperglycemia. Therefore, the aim of this study was...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664929/ https://www.ncbi.nlm.nih.gov/pubmed/26621340 http://dx.doi.org/10.1038/srep17438 |
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author | Hung, Hao-Chang Lu, Feng-Hwa Wu, Hung-Tsung Ou, Horng-Yih Yang, Yi-Ching Wu, Jin-Shang Chang, Chih-Jen |
author_facet | Hung, Hao-Chang Lu, Feng-Hwa Wu, Hung-Tsung Ou, Horng-Yih Yang, Yi-Ching Wu, Jin-Shang Chang, Chih-Jen |
author_sort | Hung, Hao-Chang |
collection | PubMed |
description | Cardiotrophin-1 is known to be a key regulator of energy homeostasis, as well as glucose and lipid metabolism in vivo. However, there are inconsistent results of the association between cardiotrophin-1 and obesity in humans, possibly confounded by hyperglycemia. Therefore, the aim of this study was to investigate the relationships among cardiotrophin-1 levels, overweight and obese individuals without diabetes in a Chinese population. The median (inter-quarter range) serum cardiotrophin-1 levels were 447.9 (230.9, 913.9), 350.6 (201.1, 666.5), and 288.1 (162.3, 572.4) pg/ml in non-diabetic subjects who were of normal weight (n = 522), overweight (n = 203), and obese (n = 93), respectively (trend test p < 0.001). Subjects who were overweight and obese had significantly lower cardiotrophin-1 levels than those with normal weight. The multivariate linear regression analyses showed that overweight (beta = −338.718, 95% CI = −552.786 ~ −124.651, p < 0.01), obese (beta = −530.275, 95% CI = −832.967 ~ −227.583, p < 0.01), and smoking (beta = −377.375, 95% CI = −654.353 ~ −100.397, p < 0.01) were negatively related to cardiotrophin-1 after adjusting for age, gender, HOMA-IR, hypertension, total cholesterol, HDL, triglyceride, eGFR, ALT, and alcohol drinking. The results of this study provided epidemiological evidence that non-diabetic subjects who were overweight or obesity had significantly lower cardiotrophin-1 concentrations than those with normal weight, and both obesity and being overweight were inversely associated with cardiotrophin-1 levels. |
format | Online Article Text |
id | pubmed-4664929 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46649292015-12-03 Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals Hung, Hao-Chang Lu, Feng-Hwa Wu, Hung-Tsung Ou, Horng-Yih Yang, Yi-Ching Wu, Jin-Shang Chang, Chih-Jen Sci Rep Article Cardiotrophin-1 is known to be a key regulator of energy homeostasis, as well as glucose and lipid metabolism in vivo. However, there are inconsistent results of the association between cardiotrophin-1 and obesity in humans, possibly confounded by hyperglycemia. Therefore, the aim of this study was to investigate the relationships among cardiotrophin-1 levels, overweight and obese individuals without diabetes in a Chinese population. The median (inter-quarter range) serum cardiotrophin-1 levels were 447.9 (230.9, 913.9), 350.6 (201.1, 666.5), and 288.1 (162.3, 572.4) pg/ml in non-diabetic subjects who were of normal weight (n = 522), overweight (n = 203), and obese (n = 93), respectively (trend test p < 0.001). Subjects who were overweight and obese had significantly lower cardiotrophin-1 levels than those with normal weight. The multivariate linear regression analyses showed that overweight (beta = −338.718, 95% CI = −552.786 ~ −124.651, p < 0.01), obese (beta = −530.275, 95% CI = −832.967 ~ −227.583, p < 0.01), and smoking (beta = −377.375, 95% CI = −654.353 ~ −100.397, p < 0.01) were negatively related to cardiotrophin-1 after adjusting for age, gender, HOMA-IR, hypertension, total cholesterol, HDL, triglyceride, eGFR, ALT, and alcohol drinking. The results of this study provided epidemiological evidence that non-diabetic subjects who were overweight or obesity had significantly lower cardiotrophin-1 concentrations than those with normal weight, and both obesity and being overweight were inversely associated with cardiotrophin-1 levels. Nature Publishing Group 2015-12-01 /pmc/articles/PMC4664929/ /pubmed/26621340 http://dx.doi.org/10.1038/srep17438 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Hung, Hao-Chang Lu, Feng-Hwa Wu, Hung-Tsung Ou, Horng-Yih Yang, Yi-Ching Wu, Jin-Shang Chang, Chih-Jen Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title | Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title_full | Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title_fullStr | Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title_full_unstemmed | Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title_short | Cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
title_sort | cardiotrophin-1 is inversely associated with obesity in non-diabetic individuals |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664929/ https://www.ncbi.nlm.nih.gov/pubmed/26621340 http://dx.doi.org/10.1038/srep17438 |
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