Breaking your leg skiing or getting a concussion from hitting your head against a drawer are all examples of how trauma can cause immediate pain and disability. What may not be so well-known is that trauma can also affect your metabolism, leading to conditions like persistent insulin resistance or even hyperglycemia, also known as high blood sugar. Such severe metabolic changes usually arise from malfunctioning white adipose tissue (WAT), the organ responsible for energy storage in the human body, but no research team had specifically investigated the role of WAT in causing metabolic dysfunction after trauma. In other words, could physical trauma cause dysfunction in WAT, leading to issues with one’s metabolism?

Scientists at the Ulm University Medical Center decided to solve this mystery. To do so, they used mice models of trauma as well as blood samples from trauma patients. For both, they noticed an increase of extracellular histones in blood samples, proteins that when found in the blood, correlated with an inflammatory response and increased cell death in WAT. Furthermore, injecting histones in the WAT of non-injured mice caused WAT inflammation and systemic hyperglycemia.

Hence, this study proposes that the metabolic sequelaes of trauma such as insulin resistance, hyperglycemia, glucose intolerance, and high plasma insulin levels could be due to inflammatory processes in WAT. By identifying the mechanism of trauma-induced metabolic dysfunction, this study lays the groundwork for identifying solutions to minimize the long-term effects of trauma. There is an urgent need for these types of studies given one-tenth of the global burden of disease is caused by injuries, and injuries remain an important cause of morbidity in developed and undeveloped countries. 

This study was performed at the Ulm University Medical Center, led by Clinical Director Julian Roose in the lab of Dr. Pamela Fischer-​Posovszky, who holds a Heisenberg Professorship in the Department of Pediatrics and Adolescent Medicine.

Managing Correspondent: Allegra Carlotta Scarpa 

Original Article: Trauma-associated extracellular histones mediate inflammation via a MYD88-IRAK1-ERK signaling axis and induce lytic cell death in human adipocytes (Nature)

Review Article: Adipose tissue: a neglected organ in the response to severe trauma? (Springer Link)

Image Credits:  iStock

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