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Poor diet can damage our blood vessels

A new study led by the University of Leipzig in Germany has found that poor diet and obesity can promote a diversity of pathologies which include vascular defects and endothelial cell (EC) dysfunctions, such as atherosclerosis, heart failure, neurodegeneration, stroke, pulmonary hypertension, renal vascular disease, microvascular dysfunction, as well as a range of hepatic vascular complications. All of these diseases are linked to vascular defects, suggesting that vascular dysfunction in obesity is a leading cause of these pathologies.

According to the experts, metabolic disease affects blood vessels in different bodily organs in unique ways. For instance, blood vessels in the liver and fat tissue struggle to process excess lipids, kidney vessels frequently develop metabolic dysfunctions, and lung vessels can become highly inflammatory.

“As vascular dysfunction drives all major pathologies, from heart failure to atherosclerosis and neurodegeneration, our research shows how bad eating habits molecularly promote the development of diverse diseases,” said study lead author Olga Bondareva, a postdoctoral researcher in Diabetes and Obesity at Leipzig.

“We want to elucidate molecular mechanisms of obesity in order to be able to offer patients tailor-made therapies in the future,” added study co-author Matthias Blüher, a professor of Molecular Endocrinology at the same university.

The scientists found that, although a healthy diet could reduce the disease-causing molecular signatures induced by a bad diet, the molecular health of blood vessels can only be improved partially. For example, while the blood vessels in the liver can recover nearly completely after dietary changes, those in the kidneys retain the disease signature, regardless of a healthy diet and major weight loss. These findings suggest that at least some of our blood vessels can develop a “memory” of metabolic disease that is quite difficult to reverse.

“Our work catalogs obesity-induced changes in the endothelium and provides the foundation for a better understanding of vascular dysfunction in metabolic disease and obesity-associated comorbidities. The molecular networks we have uncovered are candidate tissue-specific therapeutic target pathways to ameliorate EC dysfunction in a wide variety of disorders.” the authors concluded. 

The study is published in the journal Nature Metabolism.

By Andrei Ionescu, Staff Writer

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