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Published on: February 13, 2019
Sympathetic nerve-adipocyte interactions in response to acute stress
Gabryella S P Santos1, Alinne C Costa1, Caroline C Picoli1
1Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Abstract:
Psychological stress predisposes our body to several disorders. Understanding the cellular and molecular mechanisms involved in the physiological responses to psychological stress is essential for the success of therapeutic applications. New studies show, by using in vivo inducible Cre/loxP-mediated approaches in combination with pharmacological blockage, that sympathetic nerves, activated by psychological stress, induce brown adipocytes to produce IL-6. Strikingly, this cytokine promotes gluconeogenesis in hepatocytes, that results in the decline of tolerance to inflammatory organ damage. The comprehension arising from this research will be crucial for the handling of many inflammatory diseases. Here, we review recent advances in our comprehension of the sympathetic nerve-adipocyte axis in the tissue microenvironment.
Insights
Psychological stress activates sympathetic nerves, prompting brown fat cells to release IL-6. This cytokine impairs the body's ability to tolerate inflammatory damage, impacting metabolic health.
Area of Science:
- Physiology
- Immunology
- Endocrinology
Background:
- Psychological stress impacts physiological responses and disease susceptibility.
- Understanding stress-induced molecular mechanisms is key for therapeutic development.
Purpose of the Study:
- To elucidate the role of the sympathetic nerve-adipocyte axis in stress response.
- To investigate the molecular mediators linking stress to inflammatory damage tolerance.
Main Methods:
- In vivo inducible Cre/loxP systems for genetic manipulation.
- Pharmacological inhibition strategies.
- Analysis of cytokine production and metabolic pathways.
Main Results:
- Psychological stress activates sympathetic nerves, leading to IL-6 production by brown adipocytes.
- Interleukin-6 (IL-6) promotes gluconeogenesis in hepatocytes.
- This process diminishes tolerance to inflammatory organ damage.
Conclusions:
- The sympathetic nerve-adipocyte axis is a critical pathway in stress-induced metabolic dysregulation.
- IL-6 produced by adipocytes mediates the decline in inflammatory damage tolerance.
- Insights into this axis are vital for managing inflammatory diseases.
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