Dataset Information

Pericardial fat, thoracic peri-aortic adipose tissue, and systemic inflammatory marker in nonalcoholic fatty liver and abdominal obesity phenotype.

ABSTRACT: Researchers have conducted many studies about the relationships between peri-cardiovascular fat, nonalcoholic fatty liver disease (NAFLD), waist circumference, and cardiovascular disease (CVD). Nevertheless, the relationship between NAFLD and pericardial fat (PCF)/thoracic peri-aortic adipose tissue (TAT) phenotypes was still unknown. This study aimed to explore whether PCF/TAT was associated with NAFLD/abdominal obesity (AO) phenotypes in different high-sensitivity C-reactive protein (hs-CRP) levels. We consecutively studied 1655 individuals (mean age, 49.44 ± 9.76 years) who underwent a health-screening program. We showed a significant association between PCF/TAT and NAFLD/AO phenotypes in the cross-sectional study. We observed that the highest risk occurred in both abnormalities' groups, and the second highest risk occurred in the AO-only group. Subjects with AO had a significantly increased risk of PCF or TAT compared to those with NAFLD. Notably, the magnitude of the associations between PCF/TAT and NAFLD/AO varied by the level of systemic inflammatory marker (hs-CRP level). We suggested that people with AO and NAFLD must be more careful about changes in PCF and TAT. Regular measurement of waist circumference (or AO) can be a more accessible way to monitor peri-cardiovascular fat (PCF and TAT), which may serve as a novel and rapid way to screen CVD in the future.

SUBMITTER: Yun CH

PROVIDER: S-EPMC8816900 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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Pericardial fat, thoracic peri-aortic adipose tissue, and systemic inflammatory marker in nonalcoholic fatty liver and abdominal obesity phenotype.

Yun Chun-Ho CH Jhuang Jing-Rong JR Tsou Meng-Ting MT

Scientific reports 20220204 1

Researchers have conducted many studies about the relationships between peri-cardiovascular fat, nonalcoholic fatty liver disease (NAFLD), waist circumference, and cardiovascular disease (CVD). Nevertheless, the relationship between NAFLD and pericardial fat (PCF)/thoracic peri-aortic adipose tissue (TAT) phenotypes was still unknown. This study aimed to explore whether PCF/TAT was associated with NAFLD/abdominal obesity (AO) phenotypes in different high-sensitivity C-reactive protein (hs-CRP) l ...[more]

PMID: 35121786

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Project description:Thoracic aortic aneurysms result from dysregulated remodeling of the vascular extracellular matrix, which may occur as a result of altered resident cellular function. The present study tested the hypothesis that aortic fibroblasts undergo a stable change in cellular phenotype during thoracic aortic aneurysm formation.Primary murine aortic fibroblasts were isolated from normal and thoracic aortic aneurysm-induced aortas (4 weeks post induction with 0.5 mol/L CaCl(2) 15 minutes) by the outgrowth method. Normal and thoracic aortic aneurysm cultures were examined using a focused polymerase chain reaction array to determine fibroblast-specific changes in gene expression in the absence and presence of biological stimulation (endothelin-1, phorbol-12-myristate-13-acetate, angiotensin-II). The relative expression of 38 genes, normalized to 4 housekeeping genes, was determined, and genes displaying a minimum 2-fold increase/decrease or genes with significantly different normalized cycle threshold values were considered to have altered expression.At steady state, thoracic aortic aneurysm fibroblasts revealed elevated expression of several matrix metalloproteinases (Mmp2, Mmp11, Mmp14), collagen genes/elastin (Col1a1, Col1a2, Col3a1, Eln), and other matrix proteins, as well as decreased expression of Mmp3, Timp3, and Ltbp1. Moreover, gene expression profiles in thoracic aortic aneurysm fibroblasts were different than normal fibroblasts after equivalent biological stimuli.This study demonstrated for the first time that isolated primary aortic fibroblasts from thoracic aortic aneurysm-induced mice possess a unique and stable gene expression profile, and when challenged with biological stimuli, induce a transcriptional response that is different from normal aortic fibroblasts. Together, these data suggest that aortic fibroblasts undergo a stable phenotypic change during thoracic aortic aneurysm development, which may drive the enhancement of extracellular matrix proteolysis in thoracic aortic aneurysm progression.

Dataset Information

Pericardial fat, thoracic peri-aortic adipose tissue, and systemic inflammatory marker in nonalcoholic fatty liver and abdominal obesity phenotype.

Publications

Pericardial fat, thoracic peri-aortic adipose tissue, and systemic inflammatory marker in nonalcoholic fatty liver and abdominal obesity phenotype.

Similar Datasets

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