MUCNF: A natural lipid mediator in response to obesity and metabolic syndrome

A research team led by Prof. Dr. Aldo Lanza at the University of Bonn has discovered a naturally occurring lipid mediator that prevents hyperglycaemic fatty liver disease in genetically obese mice. It also suppresses the disease in the non-obese diabetic cohort. The finding opens new therapeutic strategies in the development of novel medications against metabolic syndrome and underlines the contribution of lipids in the pathophysiology of metabolic diseases.

Dr. Lanza’s team has been pursuing a New Approach to the Treatment of Type 2 Diabetes for several years now. The aim is to discover new and effective physiologic and pharmacological mechanisms that prohibit metabolic diseases of the blood-brain barrier (BBB) and to prevent verbal and physical abuse by patients with diabetes.

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Lipids are naturally occurring lipids (concentrations of lipids in cells, tissue or organs) that act as an oil-like substance in cell membranes. The perfluorocarbon derived from diet or tobacco smoke has recently been well characterized in vitro and also in vivo with regard to lipids. In the quest to date, small fraction of pharmacological action of naturally occurring lipids has not been studied in humans.

In recent years it has become obvious to many scientists that lipids play an important role in the pathological processes of insulin resistance (process for preventing and controlling excessive and unhealthy blood glucose levels). In response to increased insulin demands, the glucose in the blood drops precipitously to dangerously low levels. Insulin resistance is abnormal as it is due to a combination of genetic and environmental factors. The oxidative stress somehow perpetuates these metabolic unfavorable reactions (osteosclerosis), resulting in hyperglycaemia (peroxisomes). To date, the use of drugs that activate lipids on the BBB has been unsuccessful in normal rodents.

The chronic inflammation experienced by insulin resistance can be put down to many changes in our body. Lanza’s observation that lipids are particularly liked in the pathogenesis of metabolic syndrome (hyperglycaemic fatty liver disease) raises the possibility that an enzymatic pathway also plays an important role in the pathogenesis of metabolic syndromes. “The first indication that lipids can be used as a natural substance for the prevention of atherosclerosis had already been made way back in the 1950s by Lanza’s team. However, studies with experimental animals now indicate that the first team with evidence indicating lipids as a naturally occurring lipid mediator could not have been produced in existence today,” explains Lanza.

However, her team developed a molecular target molecule that binds to lipids in the pathophysiological processes of type 2 diabetes instead of by the enzymes of the blood fluids. In a transgenic mouse model studied in collaboration with Lanza’s team, the investigators were able to achieve a superscription of the target protein. “Our results show that the target protein does not work anymore under normal states of metabolism. This indeed surprises us. We expected that the protein would reach an irreversible end point and would thenceforth no longer be effective in suppressing autophagy. Such unexpected endpoints may be of therapeutic relevance in the future,” says Lanza. “As a result, lipids may prove to represent a candidate in organ development investments: They cause less inflammation on their own. This totally opens up new possibilities for therapeutic possibilities against diabetes and might be a helpful therapeutic target for obesity and metabolic syndromes.”