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Serum apoptotic marker M30 is positively correlated with early diastolic dysfunction in adolescent obesity

Authors :
Yu-Tsun Su
Hsien-Kuan Liu
Jiunn-Ren Wu
Ming-Chun Yang
Ching-Chung Tsai
Source :
PLoS ONE, Vol 14, Iss 5, p e0217429 (2019), PLoS ONE
Publication Year :
2019
Publisher :
Public Library of Science (PLoS), 2019.

Abstract

Purpose Obesity in adolescence has been shown to be related to cardiac geometric and functional changes. Cardiac dysfunction in adults with obesity could be attributed to chronic low-grade inflammation, apoptosis of cardiomyocyte, and glucose metabolic disorder. The aforementioned association in adolescents with obesity have never been well studied. Our aim was to determine the types of cardiac dysfunction in adolescents with obesity and survey the association between cardiac dysfunction and chronic low-grade inflammation, apoptosis, and glucose dysregulation in adolescents with obesity. Methods Adolescents aged between 10 and 20 years were enrolled in this study. Body mass index, waist-to-hip ratio, blood pressure, glucose metabolism, and high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-α), and apoptosis marker M30 levels were measured. Echocardiographic indices were also measured. The association between serum biomarkers and echocardiographic function parameters was analyzed. Results Diastolic dysfunction was the major finding in the cardiac functional assessment. The main changes in glucose metabolism were elevated C-peptide level and insulin resistance. Hs-CRP, IL-6, and M30 levels also increased with adolescent obesity. M30 was the major biomarker that was highly correlated to diastolic dysfunction indices in adolescents with obesity. Conclusions Diastolic dysfunction was the main change in adolescent obesity. Insulin resistance, apoptotic marker M30, hs-CRP, and IL-6 were all elevated in adolescents with obesity. Only M30 was related to indices of left ventricular diastolic dysfunction among adolescents with obesity, rather than inflammation or insulin resistance.

Details

ISSN :
19326203
Volume :
14
Database :
OpenAIRE
Journal :
PLOS ONE
Accession number :
edsair.doi.dedup.....658aa7ff9f9b341d2fe55ca1125968cf