A team of researchers discovered that metabolic disorder affects blood arteries in various organs of our body in a unique way. Blood vessels in the liver and adipose tissue, for example, fail to handle excess lipids; kidney vessels develop metabolic malfunction; lung arteries become highly inflammatory; and transport between brain vasculature is impaired.
“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 Dr Olga Bondareva, the first author of the study.
“We want to elucidate molecular mechanisms of obesity in order to be able to offer patients tailor-made therapies in the future,” said HI-MAG director Professor Matthias Bluher.
For years, the speaker of Collaborative Research Centre 1052 Obesity Mechanisms has been performing morbid obesity research at Leipzig University. The current investigation includes experts from Leipzig who work in cardiology and laboratory medicine. The researchers next investigated whether a good diet may diminish disease-causing molecular markers caused by a poor diet.
They discovered that a good diet can, but only marginally, enhance the molecular health of blood arteries. For example, despite a healthy diet and considerable weight loss, blood vessels in the liver healed nearly entirely, whereas blood vessels in the kidneys preserved the illness characteristic. This implies that certain of our blood vessels might form a “memory” of metabolic illness that is difficult to repair.
Leipzig Obesity Research
For many years, the mechanisms and treatment of obesity have been a focus of academic study in Leipzig. There is a broad research landscape dedicated to the disease’s prevention and treatment. Obesity research at Leipzig covers a wide variety of themes, including genetic links, metabolic problems, fat storage processes, the involvement of the brain in eating, and therapeutic approaches for decreasing and maintaining weight.