In this process, the crucial step of the signaling pathway is controlled by autotaxin, an enzyme that is responsible for the production of lysophosphatidic acid (LPA) in the brain as a modulator of network activity. Administering autotaxin inhibitors can thereby significantly reduce both excessive food intake after fasting and obesity in animal models.
Eating disorders, particularly obesity, are among the leading causes of a wide range of diseases in industrialized societies across the world, especially cardiovascular diseases with lifelong disabilities or fatal outcomes such as heart attacks, diabetes, or strokes. According to a Robert Koch Institute report from 2021, 67 percent of men and 53 percent of women in Germany are overweight. 23 percent of adults are severely overweight (obese). Attempts to influence eating behavior with medication have so far proved unsuccessful. A novel therapy that modulates the excitability of networks that control eating behavior might be a game changer in the worldwide fight against obesity.
The team of researchers discovered an increased rate of obesity and the attendant type II diabetes in people with impaired synaptic LPA signaling. A group led by Professor Johannes Vogt (Faculty of Medicine, University of Cologne), Professor Robert Nitsch (Faculty of Medicine, University of Münster) and Professor Thomas Horvath (Yale School of Medicine, New Haven, USA) has now shown that control of the excitability of neurons in the cerebral cortex by LPA plays an essential role in the control of eating behavior: AgRP neurons regulate the amount of lysophosphatidylcholine (LPC) in the blood. Through active transport, LPC reaches the brain, where it is converted by the enzyme autotaxin (ATX) into LPA, which is active at the synapse. Synaptic LPA signals stimulate specific networks in the brain, thus leading to increased food intake.
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Category(s):Eating Disorders
Source material from SciTechDaily
