Subclinical vascular inflammation in subjects with normal weight obesity and its association with body fat: an 18 F-FDG-PET/CT study.
Subclinical vascular inflammation in subjects with normal weight obesity and its association with body fat: an 18 F-FDG-PET/CT study.
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DOI：
10.1186/1475-2840-13-70
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发表时间：
2014-04-04
影响因子：
9.3
通讯作者：
Ahn CW
中科院分区：
文献类型：
--
作者：
Kang S;Kyung C;Park JS;Kim S;Lee SP;Kim MK;Kim HK;Kim KR;Jeon TJ;Ahn CW
虽然体重指数（BMI）是定义肥胖的最广泛接受的参数，但最近的研究表明，一组独特的患者表现出正常BMI和过量体脂（BF），这被称为正常体重肥胖（NWO）。BF增加是动脉粥样硬化的既定危险因素。然而，目前尚不清楚与正常体重瘦（NWL）受试者相比，NWO受试者是否已经具有更高程度的血管炎症;此外，BF与正常体重受试者中血管炎症的关联在很大程度上是未知的。从在自我推荐的医疗保健促进计划中接受18 F-氟脱氧葡萄糖正电子发射断层扫描/计算机断层扫描（18 F-FDG-PET/CT）的连续招募患者的3年数据库中确定无任何重大血管疾病史的NWO和NWL受试者（每组n = 82）。亚临床血管炎症的程度通过18 F-FDG-PET/CT（一种用于评估血管炎症的无创工具）测量的颈动脉的平均和最大靶-背景比（TBRmean和TBRmax）进行评估。我们发现NWO受试者的代谢失调比NWL受试者更严重，血压显著升高，空腹血糖水平升高，血脂水平更差。此外，NWO受试者表现出比NWL受试者更高的TBR（TBRmean：1.33 ± 0.16 vs 1.45 ± 0.19，p < 0.001; TBRmax：1.52 ± 0.23 vs 1.67 ± 0.25，p < 0.001）。TBR与总BF显著相关（TBRmean：r = 0.267，p = 0.001; TBRmax：r = 0.289，p < 0.001），年龄（TBRmean：r = 0.170，p = 0.029; TBRmax：r = 0.165，p = 0.035），BMI（TBRmean：r = 0.184，p = 0.018; TBRmax：r = 0.206，p = 0.008）和空腹血糖水平（TBRmean：r = 0.157，p = 0.044; TBRmax：r = 0.182，p = 0.020）。在多元线性回归分析中，校正年龄、BMI和空腹血糖水平后，BF是TBRmean和TBRmax的独立决定因素（TBRmean：回归系数= 0.020，p = 0.008; TBRmax：回归系数= 0.028，p = 0.005）。与NWL相比，调整混杂因素后，NWO也与TBRmax值升高独立相关（比值比= 2.887，95%置信区间1.206-6.914，p = 0.017）。NWO与更高程度的亚临床血管炎症相关，其中BF是主要的促成因素。这些结果保证了NWO患者亚临床动脉粥样硬化的研究。
Although body mass index (BMI) is the most widely accepted parameter for defining obesity, recent studies have indicated a unique set of patients who exhibit normal BMI and excess body fat (BF), which is termed as normal weight obesity (NWO). Increased BF is an established risk factor for atherosclerosis. However, it is unclear whether NWO subjects already have a higher degree of vascular inflammation compared to normal weight lean (NWL) subjects; moreover, the association of BF with vascular inflammation in normal weight subjects is largely unknown. NWO and NWL subjects (n = 82 in each group) without any history of significant vascular disease were identified from a 3-year database of consecutively recruited patients undergoing 18 F-fluorodeoxyglucose positron emission tomography/computed tomography (18 F-FDG-PET/CT) at a self-referred Healthcare Promotion Program. The degree of subclinical vascular inflammation was evaluated using the mean and maximum target-to-background ratios (TBRmean and TBRmax) of the carotid artery, which were measured by 18 F-FDG-PET/CT (a noninvasive tool for assessing vascular inflammation). We found that metabolically dysregulation was greater in NWO subjects than in NWL subjects, with a significantly higher blood pressure, higher fasting glucose level, and worse lipid profile. Moreover, NWO subjects exhibited higher TBR than NWL subjects (TBRmean: 1.33 ± 0.16 versus 1.45 ± 0.19, p < 0.001; TBRmax: 1.52 ± 0.23 versus 1.67 ± 0.25, p < 0.001). TBR was significantly associated with total BF (TBRmean: r = 0.267, p = 0.001; TBRmax: r = 0.289, p < 0.001), age (TBRmean: r = 0.170, p = 0.029; TBRmax: r = 0.165, p = 0.035), BMI (TBRmean: r = 0.184, p = 0.018; TBRmax: r = 0.206, p = 0.008), and fasting glucose level (TBRmean: r = 0.157, p = 0.044; TBRmax: r = 0.182, p = 0.020). In multiple linear regression analysis, BF was an independent determinant of TBRmean and TBRmax, after adjusting for age, BMI, and fasting glucose level (TBRmean: regression coefficient = 0.020, p = 0.008; TBRmax: regression coefficient = 0.028, p = 0.005). Compared to NWL, NWO was also independently associated with elevated TBRmax values, after adjusting for confounding factors (odds ratio = 2.887, 95% confidence interval 1.206–6.914, p = 0.017). NWO is associated with a higher degree of subclinical vascular inflammation, of which BF is a major contributing factor. These results warrant investigations for subclinical atherosclerosis in NWO patients.
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影响因子：
16.2
作者：
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通讯作者：
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DOI：
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动脉粥样硬化的炎症。
DOI：
10.1161/atvbaha.108.179705
发表时间：
2012-09
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
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作者：
Libby P
通讯作者：
Libby P