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The highest quartile for pericardial fat volumes was associated with the highest odds of restrictive lung patterns [odds ratio 1. The authors suggested that the paracrine effects of pericardial fat on the lungs and the mechanical effects of pericardial fat were associated with a restrictive lung pattern; however, the exact underlying causes remain unclear.
On the contrary, this study showed that intrathoracic fat volume in males had a statistically significant association with decreased lung function, whereas pericardial fat volume exhibited no such association.
One of the reasons might be the difference in biochemical properties between intrathoracic fat and pericardial fat. Intrathoracic fat and pericardial fat have different embryogenic origins: intrathoracic fat originates from the primitive thoracic mesenchyme; whereas pericardial fat originates from the splanchnopleuric mesoderm A higher pericardial fat volume suggests an association with risk factors for cardiovascular diseases and increased severity of coronary artery disease because of its biochemical nature, increased expression of inflammatory cytokines interleukin-6 and tumor necrosis factor-a, among others , decreased concentrations of adiponectin, and its location feature, adjacent to the coronary artery Meanwhile, in some previous studies, a group of subjects with metabolic syndrome exhibited higher intrathoracic fat volumes on chest magnetic resonance imaging than a group of subjects without metabolic syndrome, with no differences in pericardial fat volume between the two groups Furthermore, intrathoracic fat volumes positively correlated with visceral abdominal fat volumes 26 and were inversely associated with lung function 27 , Although the impact of increases in intrathoracic fat is less known, considering its anatomical proximity to the lung, intrathoracic fat could have a more significant effect on lung function as compared with pericardial fat.
This study demonstrated that increment of both intrathoracic fat and visceral abdominal fat volumes were significantly associated with reduced lung function in males. These results suggest that the role of intrathoracic fat in the prediction of decreased lung function in males should be reconsidered.
Given that subcutaneous fat envelops almost the entire thoracic cage and shows a lower expression of inflammatory genes and cytokine secretion when compared with pericardial fat volume, subcutaneous thoracic fat might be associated with decreased lung function due to mechanical effects 24 , However, a previous study reported that subcutaneous thoracic fat volume calculated on axial chest CT slices was positively associated with CRP levels and systemic adiposity markers such as BMI and fat-free masses in females These previous results suggest that subcutaneous thoracic fat also has metabolic effects.
In this study, all types of visceral fat volumes were higher in males; whereas subcutaneous fat volumes were higher in females. These findings confirmed the notion that women have a higher percentage of total adipose tissue, lower visceral fat, and higher subcutaneous fat in the lower extremities than men These gender-related differences in body fat distribution might induce differences in cardiometabolic risk and lung function.
Although lung functions of both sexes were commonly affected by subcutaneous thoracic fat volumes through mechanical effects, lung function in males who have higher visceral fat volume might be more vulnerable to metabolic effects than in females.
It has been established that traditional adiposity indices, including BMI, waist circumference, and body fat percentage, are significantly related to lung function 32 , Neither body fat percentage nor BMI alone is reliable measurements to identify specific risk factors for the pathogenesis of diseases and can fully reflect the characteristics of body fat distribution.
Compared with the traditional uses of body fat percentage, BMI or waist circumference, these direct measurements of fat volumes using CT or magnetic resonance imaging could provide more relevant information for understanding the pathophysiology of pulmonary according to sex, especially in males, and help show the correlation between lung diseases and other cardiovascular and metabolic diseases.
This study had some limitations. First, we used pulmonary function test data acquired from subjects who underwent a previously planned health-screening program.
The data did not include total lung capacity, residual volume, and diffusing capacity of the lungs, as well as lung function after bronchodilator intake. The absence of these additional data made it challenging to determine lung function accurately. However, this study may represent a population without respiratory diseases that have normal or nearly normal lung function.
Second, there was no consensus on a specific protocol for the measurement of subcutaneous thoracic fat. Therefore, we selected the boundary of measurements using the scapular bone as a reference point similar to those measured in another study Finally, although significant effort into maintaining a standard body position for CT scanning was attempted, some variations could have influenced the accuracy of the measurements.
Including all types of thoracic fat, these findings suggest that the volumes of local thoracic fat deposits were inversely associated with lung function.
In addition, while subcutaneous thoracic fat volumes demonstrated the same effects in both sexes, there were sex-related differences as predictors of lung function that suggest the important roles of intrathoracic fat and visceral abdominal fat volumes in males.
Future investigations involving larger cohorts and longitudinal studies are needed to evaluate the exact cause-and-effect relationship between local adiposity and lung function impairment.
This study may implicate further studies examining the association between local fat deposits and impaired lung function diseases such as chronic obstructive pulmonary disease, asthma, and interstitial lung disease, in which the effects of fat on lung function would be more significant.
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Tonstad S, Sandvik E, Larsen PG, Thelle D. Gender differences in the prevalence and determinants of the metabolic syndrome in screened subjects at risk for coronary heart disease. Download references. The authors thank all the subjects who participated in the study and the hospital staffs for their contribution in sample and data collection.
This study was supported by National Natural Science Foundation of China , , Shanghai Municipal Health Commission Department of Endocrinology, Xinhua Hospital Chongming Branch, School of Medicine, Shanghai Jiaotong University, 25 Nanmen Road, Shanghai, China.
Department of Endocrinology, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Kongjiang Road, Shanghai, , China. You can also search for this author in PubMed Google Scholar. Q and Q. S conceived and designed the study. Y, XY. L and HX. G contributed to discussion and collected the data.
S analyzed the data. H wrote the paper. All authors read and approved the final manuscript. Correspondence to Qing Su or Li Qin. The study protocol was approved by the ethics committee of Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine. All participants in the present analysis gave written informed consent before they participated in this study.
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He, S. et al. Visceral adiposity index is associated with lung function impairment: a population-based study. Respir Res 22 , 2 Download citation. Received : 20 August Accepted : 10 December Published : 06 January Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Background The effects of visceral adiposity on decreased lung function have drawn much attention.
Methods We collected data from a population-based study of subjects aged 40 years or older. Conclusions We were the first to show a clear correlation between the VAI and lung function impairment in the Chinese population.
Introduction Impaired pulmonary function is a predictor of mortality related to various diseases independent of diagnosed lung disease and smoking status [ 1 ]. Materials and methods Study population This study is a part of the Risk Evaluation of Cancer in Chinese Diabetic Individuals: a longitudinal REACTION study, which was a community study conducted among adults aged 40 years and older.
Data collection Essential information on demographic characteristics e. Lung function measurements Lung function tests, including forced vital capacity FVC and forced expiratory volume in 1 s FEV1 , were conducted by a trained physician using an electronic spirometer Model BF-II, Jintan, China.
Results Demographic and clinical characteristics of the study population The total of participants aged 40—79 years were included, with men and women.
Table 1 Demographic and clinical characteristics of the study population Full size table. Full size image. Table 2 Lung function in different quartiles of VAI Full size table.
Discussion In the present study, we investigated the relationship of the VAI with pulmonary dysfunction among a Chinese middle-aged and elderly population.
Availability of data and materials The data that support the findings of this study are available from REACTION Study Group but restrictions apply to the availability of these data, which were used under license for the current study, and so are not publicly available.
Abbreviations VAI: Visceral adiposity index VAT: Visceral adipose tissue SAT: Subcutaneous adipose tissue WC: Waist circumference BMI: Body mass index TGs: Triglycerides TC: Total cholesterol HDL-c: High-density lipoprotein cholesterol LDL-c: Low-density lipoprotein cholesterol SBP: Systolic blood pressure DBP: Diastolic blood pressure FPG: Fasting plasma glucose HbA1c: Hemoglobin A1c RIA: Radioimmunoassay UA: Uric acid SCr: Serum creatinine eGFR: Estimated glomerular filtration rate FVC: Forced vital capacity FEV1: Forced expiratory volume in 1 s.
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