Centre de Recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Québec, Canada.
Centre Hospitalier Universitaire de Grenoble-Alpes, Laboratoire HP2 INSERM U 1042 Université Grenoble-Alpes, Grenoble, France.
PLoS One. 2020 Apr 10;15(4):e0231072. doi: 10.1371/journal.pone.0231072. eCollection 2020.
A high prevalence of intermediate cardiometabolic risk factors and obesity in chronic obstructive pulmonary disease (COPD) has suggested the existence of pathophysiological links between hypertriglyceridemia, insulin resistance, visceral adiposity, and hypoxia or impaired pulmonary function. However, whether COPD contributes independently to the development of these cardiometabolic risk factors remains unclear. Our objective was to compare ectopic fat and metabolic profiles among representative individuals with COPD and control subjects and to evaluate whether the presence of COPD alters the metabolic risk profile. Study participants were randomly selected from the general population and prospectively classified as non-COPD controls and COPD, according to the Global Initiative for Chronic Obstructive Lung Disease classification. The metabolic phenotype, which consisted of visceral adipose tissue area, metabolic markers including homeostasis model assessment of insulin resistance (HOMA-IR), and blood lipid profile, was obtained in 144 subjects with COPD and 119 non-COPD controls. The metabolic phenotype was similar in COPD and controls. The odds ratios for having pathologic values for HOMA-IR, lipids and visceral adipose tissue area were similar in individuals with COPD and control subjects in multivariate analyses that took into account age, sex, body mass index, tobacco status and current medications. In a population-based cohort, no difference was found in the metabolic phenotype, including visceral adipose tissue accumulation, between COPD and controls. Discrepancies between the present and previous studies as to whether or not COPD is a risk factor for metabolic abnormalities could be related to differences in COPD phenotype or disease severity of the study populations.
在慢性阻塞性肺疾病（COPD）中，中间型心血管代谢危险因素和肥胖症的高患病率表明，高甘油三酯血症、胰岛素抵抗、内脏肥胖症、缺氧或肺功能障碍之间存在病理生理联系。然而，COPD 是否独立导致这些心血管代谢危险因素的发展仍不清楚。我们的目的是比较具有代表性的 COPD 患者和对照个体的异位脂肪和代谢特征，并评估 COPD 的存在是否改变了代谢风险特征。研究参与者是从一般人群中随机选择的，并根据全球慢性阻塞性肺疾病倡议（GOLD）分类，前瞻性地分为非 COPD 对照组和 COPD 组。在 144 例 COPD 患者和 119 例非 COPD 对照组中获得了代谢表型，包括内脏脂肪组织面积、代谢标志物（包括稳态模型评估的胰岛素抵抗指数（HOMA-IR））和血脂谱。在考虑年龄、性别、体重指数、吸烟状态和当前药物治疗的多变量分析中，COPD 患者和对照组患者的 HOMA-IR、血脂和内脏脂肪组织面积的病理值的比值相似。在基于人群的队列中，COPD 组和对照组之间的代谢表型（包括内脏脂肪组织堆积）没有差异。目前的研究与之前的研究在 COPD 是否是代谢异常的危险因素方面存在差异，这可能与研究人群中 COPD 表型或疾病严重程度的差异有关。
