Today, insulin injections are essential for the survival of patients with type 1 diabetes or a severe form of type 2 diabetes. However, this treatment is not without risk: overdose can trigger hypoglycaemia, i.e. a drop in blood glucose levels that can lead to coma or even death. But underdosed, it can lead to equally dangerous hyperglycaemia. In addition, insulin is involved in the control of ketones, elements that are produced when the liver breaks down lipids in the absence of sufficient glucose reserves, which become toxic in too large quantities. In addition, long-term insulin treatments cause excess fat and cholesterol in the blood and therefore increases the risk of cardiovascular disease.
As early as 2010, Roberto Coppari's team, a professor at the Diabetes Centre of the UNIGE Faculty of Medicine, highlighted the gluco- and lipid-regulatory properties of leptin, a hormone involved in hunger control. "However, leptin has proved difficult to use pharmacologically in human beings due to the development of leptin resistance," says Roberto Coppari. "In order to overcome this problem, we shifted our focus on the metabolic mechanisms triggered by leptin rather than on the hormone itself."
Scientists - Changes - Blood - Mice - Leptin
The scientists observed changes in the blood of insulin-deficient mice to whom they administered leptin and noted the abundant presence of the S100A9 protein. "This protein has a bad reputation because, when it binds to its sister protein S100A8, it creates a complex called calprotectin that causes the symptoms of many inflammatory or autoimmune diseases," says Giorgio Ramadori, a researcher at the Diabetes Centre of the UNIGE Faculty of Medicine and the first author of this work. "However, by over-expressing S100A9, we can, paradoxically, reduce its harmful combination with S100A8, hence dampening calprotectin levels."
The researchers then administered high doses of S100A9 to their insulin-deficient...
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