Department of Anesthesiology, University of Vermont, Burlington, Vermont, United States.
Department of Medicine, University of Vermont, Burlington, Vermont, United States.
Am J Physiol Lung Cell Mol Physiol. 2024 Nov 1;327(5):L615-L623. doi: 10.1152/ajplung.00112.2024. Epub 2024 Sep 10.
Obesity may lead to pulmonary dysfunction through complex and incompletely understood cellular and biochemical effects. Altered lung lipid metabolism has been identified as a potential mechanism of lung dysfunction in obesity. Although murine models of obesity demonstrate changes in pulmonary surfactant phospholipid composition and function, data in humans are lacking. We measured untargeted shotgun lipidomes in two bronchoalveolar lavages (BALs) from apical and anteromedial pulmonary subsegments of 14 adult subjects (7 males and 7 females) with body mass indexes (BMIs) ranging from 24.3 to 50.9 kg/m. The lipidome composition was characterized at the class, species, and fatty acyl/alkyl level using total lipid molecular ion signal intensities normalized to BAL protein concentration and epithelial lining fluid volumes. Multivariate analyses were conducted to identify potential changes with increasing BMI. The alveolar lipidomes contained the expected composition of surfactant-associated phospholipids, sphingolipids, and sterols in addition to cardiolipin and intracellular signaling lipid species. No significant differences in lipidomes were detected between the two BAL regions. Though a small number of lipid species were associated with BMI in multivariate analyses, no robust differences in lipidome composition or specific lipid species were identified over the range of body habitus. The magnitude of obesity alone does not substantially alter the alveolar lipidome in patients without lung disease. Differences in lung function in patients with obesity and no lung disease are unlikely related to changes in alveolar lipid composition. Altered lung lipid metabolism has been identified as a potential mechanism of lung dysfunction in obesity, but data in humans are lacking. We measured the alveolar lipidome in bronchoalveolar lavages from subjects with healthy lungs with a wide range of body mass index. There were no differences in lipidome composition in association with the magnitude of obesity. In patients with healthy lungs, obesity alone does not alter the alveolar lipidome.
肥胖可能通过复杂且尚未完全了解的细胞和生化作用导致肺功能障碍。改变肺脂质代谢已被确定为肥胖导致肺功能障碍的潜在机制。尽管肥胖的啮齿动物模型显示肺表面活性剂磷脂组成和功能发生变化，但人类的数据却缺乏。我们在 14 名成年受试者（7 名男性和 7 名女性）的两个支气管肺泡灌洗液（BAL）中测量了非靶向性 shotgun 脂质组学，这些受试者的体重指数（BMI）范围从 24.3 到 50.9kg/m。使用 BAL 蛋白浓度和上皮衬里液体积标准化的总脂质分子离子信号强度，在类、种和脂肪酸/烷基水平上对脂质组学组成进行了特征描述。进行了多变量分析以确定随着 BMI 增加的潜在变化。肺泡脂质组学除了心磷脂和细胞内信号脂质外，还包含了预期的表面活性剂相关磷脂、鞘脂和甾醇组成。在两个 BAL 区域之间未检测到脂质组学的显着差异。尽管在多变量分析中，有少数脂质与 BMI 相关，但在身体形态范围内，脂质组学组成或特定脂质种类没有明显差异。单纯肥胖的程度不会使无肺部疾病患者的肺泡脂质组学发生实质性改变。肥胖而无肺部疾病患者的肺功能差异不太可能与肺泡脂质组成的变化有关。改变肺脂质代谢已被确定为肥胖导致肺功能障碍的潜在机制，但人类的数据却缺乏。我们测量了来自肺部健康、BMI 范围广泛的受试者的支气管肺泡灌洗液中的肺泡脂质组学。与肥胖程度相关的脂质组学组成没有差异。在肺部健康的患者中，单纯肥胖不会改变肺泡脂质组学。
