Recent Molecular Link Between Anxiety, Metabolism May Impact Inflammatory Response

Recent Molecular Link Between Anxiety, Metabolism May Impact Inflammatory Response

Molecular elements that link anxiety and metabolism were recently described by a group of researchers from the Hebrew University of Jerusalem. The knowledge sheds light on how anxiety and metabolism impact inflammation that can further affect chronic disorders such as Crohn’s disease via a type of microRNA with shared biological mechanisms.

Metabolic and anxiety-related disorders have been subjects of scientific research and therapeutic targeting for several decades. Links between the two have long been suspected of overlapping.

Hermona Soreq, lead researcher and a professor of the Edmond and Lily Safra Center for Brain Sciences and the Department of Biological Chemistry at the Faculty of Mathematics and Sciences, said the “connection between body and mind, between the physical and emotional” were already known. Studies show that psychological trauma affects gene activity.

“Our previous research found a link between microRNA and stressful situations — stress and anxiety generate an inflammatory response and dramatically increase the expression levels of microRNA regulators of inflammation in both the brain and the gut, for example the situation of patients with Crohn’s disease may get worse under psychological stress,” Soreq said.

For the current study the researchers added obesity to the equation.

“We revealed that some anxiety-induced microRNA are not only capable of suppressing inflammation but can also potentiate metabolic syndrome-related processes. We also found that their expression level is different in diverse tissues and cells, depending on heredity and exposure to stressful situations,” said  Soreq in a press release.

MicroRNA Regulators of Anxiety and Metabolic Disorders,” published in the journal Trends in Molecular Medicine, reports on the specific microRNA mechanisms involved in controlling regulatory networks shared by metabolic and anxiety-related conditions.

In particular, the authors detail evidence that microRNAs shown to be involved in the disorders are also regulators of acetylcholine signaling in the nervous system, and of its related molecular mechanics. This is of particular relevance because the molecular signaling systems had been previously related to anxiety-prone states and were also identified as important inflammatory suppressors.

Previously considered as “junk-DNA,” microRNAs are small RNA elements included in the human genome. They are now recognized as important regulators of proteins production and stability.

“The discovery has a diagnostic value and practical implications, because the activity of microRNAs can be manipulated by DNA-based drugs,” Soreq said. “It also offers an opportunity to reclassify ‘healthy’ and ‘unhealthy’ anxiety and metabolic-prone states, and inform putative strategies to treat these disorders.”

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