Which factor contributes to post-burn hyperglycemia due to muscle catabolism?

In the context of post-burn hyperglycemia, muscle catabolism significantly contributes to an increased release of glucose into the bloodstream. When the body experiences burns, especially extensive ones, it enters a hypermetabolic state where energy expenditure rises. During this phase, the body prioritizes energy for healing and sustaining the metabolic demands associated with trauma.

Muscle catabolism refers to the breakdown of muscle tissue, which releases amino acids into circulation. Some of these amino acids can be converted to glucose through a process known as gluconeogenesis, commonly occurring in the liver. As muscle tissue is broken down, it not only depletes muscle mass but also increases the availability of substrates that can be converted to glucose, exacerbating hyperglycemia.

While insulin resistance may play a role in post-burn conditions, the primary mechanism associated with increased glucose levels in this situation is directly correlated with muscle catabolism. Hormonal imbalances and factors like increased appetite may exist but are not as directly tied to the metabolic pathway that results in hyperglycemia when considering muscle breakdown specifically. Hence, the correct identification of glucose uptake impairment in the context of muscle catabolism reveals a direct link to the complexity of metabolic changes following severe burns.