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Metformin Attenuates Hepatic Mitochondrial Dysfunction and Oxidative Stress in a Model of Burn Injury

Thibacg Sivayoganathan

TSpace (University of Toronto), 2018

1 citation

Abstract

Elderly burn patients are a high-risk group with poor survival rates. The incidence of organ failure for elderly burns is particularly high, and the organs typically affected, such as the liver, are mitochondria rich. This suggests that mitochondria underly the vulnerability of the elderly to burns, and thus treatments directly targeting mitochondria, such as metformin, may improve their outcome. Thus, we hypothesize that the elderly have a worse outcome due to faulty hepatic mitochondria and that metformin intervention would enable recovery. Our data shows that while adult murine mitochondria rebound from the initial insult, older animals display delayed recovery of mitochondrial bioenergetics. Moreover, metformin treatment suppresses the hypermetabolic mitochondria of the younger cohort while significantly increasing respiration in the aged group. These findings suggest that aging leads to a failure to normalize hepatic mitochondria after trauma and that metformin is a possible agent that can restore mitochondrial responses to burns.

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Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence.

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