“These changes in lung tissue are similar to those that normally occur with age and suggest that being overweight causes the lungs to ‘age’ prematurely,” they said in the paper published in the journal Cell Reports. The team used state-of-the-art multi-omics approaches to simultaneously examine proteins, fats, and genes for specific questions. They combined this analysis with microscopic image analyses and experiments that show how the lungs actually work.
The researchers compared the lungs of obese and lean mice, analysed human connective tissue cells in the lungs, and took a close look at the composition of the lungs -- enabling them to understand both molecular and functional changes. In obesity, lung fibroblasts, that is, connective tissue cells, specifically accumulate fat, become more mobile, and show early signs of premature ageing. At the same time, the matrisome, the "scaffolding" of the lung, changes, and the balance of certain protease inhibitors is disrupted, the researchers said.
“These changes make the lungs less elastic, which could explain why obesity is often associated with breathing difficulties,” they noted. Interestingly, these changes are similar to those normally seen in older people -- pointing to obesity as a driver of accelerated lung ageing. One of the biggest challenges was developing methods to analyse the complex connective tissue of the lungs -- the fibroblastic stroma (FSCs) -- which consists of many different cell types. In addition, the extracellular matrix is also difficult to study because many of its proteins are insoluble and have a very complex structure, the team said. “Overall, obesity led to complex alterations in the lung that ultimately affect FSCs and suggest that overnutrition may act as a contributor to premature ageing, thereby compromising lung health,” the researchers said.
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