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A recent study from the University of Gothenburg sheds light on a newly discovered mechanism that may explain why some individuals with obesity develop type 2 diabetes while others do not. The research explores the disrupted function of immune system cells, known as macrophages, responsible for cleaning up collagen fragments during weight gain. The findings, primarily based on experiments in mice, suggest that this mechanism also applies to humans and could provide crucial insights into preventing or treating type 2 diabetes.
The study, published in the journal PNAS, delves into the relationship between obesity, insulin resistance, and the breakdown of collagen, a structural protein found in adipose tissue. Weight gain prompts the degradation of collagen to accommodate growing fat cells, a process managed by macrophages. However, the study reveals that this crucial function of macrophages is impaired in obesity and insulin resistance, leading to the accumulation of collagen fragments in adipose tissue.
The breakdown of collagen involves a highly regulated process where fragments are enzymatically degraded outside fat cells and then engulfed by macrophages for complete degradation. In obesity, this mechanism is deactivated, causing collagen fragments to accumulate. Previously considered debris, the study indicates that these fragments actively influence cellular processes such as inflammation and cell division, transitioning from maintaining normal adipose tissue function to becoming pathogenic.
The research team, led by Professor Ingrid Wernstedt Asterholm, conducted experiments on mice and exposed human macrophages to diabetes-like conditions, demonstrating the loss of their ability to effectively “clean up” collagen. Asterholm suggests that the deactivation of this mechanism might occur when adipose tissue reaches a certain genetically determined degree of adiposity.
The study holds promise for developing new strategies to prevent or treat type 2 diabetes. Additionally, collagen fragments could serve as measurable biological markers, potentially identifying individuals at a higher risk of developing the disease. As the link between obesity, disrupted cellular functions, and diabetes becomes clearer, the findings pave the way for targeted interventions and personalized approaches to manage metabolic health.
