Mediating burn-induced gastric impairment with insulin treatment

I'm trying to think my way through some of the results in Mechanisms of burn-induced impairment in gastric slow waves and emptying in rats by Sallam et al. This article (like almost all of the articles I talk about on this blog) is outside of my subfield in physiology, so I'm trying to apply the little that I know about gastro and immune physiology in order to get this to make sense.

It is established that severe skin burns result in decreased gut motility and clearance, likely due to sympathetic nervous system and immune system pathways. Flesh wounds typically activate the fight or flight response, which floods the blood with glucose for readily-available energy and also decreases gut motility in order to reduce the amount of energy being used by areas of the body not involved in immediate survival. The immune system has similar effects via different pathways. The end result is a rise in blood glucose (hyperglycemia) that I would assume is used for energy to repair or rebuild the injured tissue, which is an energetically expensive process. These effects are supplemented by the effects of stress endocrines, which also act to increase blood glucose levels, and possibly growth endocrines as well (I don't know enough about the inflammation response to know if growth endocrines are responsible for the rebuilding of injured tissues, but I would imagine that they are). Additionally, when the skin barrier has been compromised, it would make sense to me that the body would want to be in a post-absorptive state, so that areas of the body not involved in repairing the injury site will run off of ketones and reduce the fuel available for pathogens that may get in through the compromised barrier.

What I gather from this is that in response to a severe skin burn, a) the body shuts (or slows) down the gastrointestinal tract in order to conserve energy for repair and to force the body into a post-absorptive state and b) various systems in the body act to induce hyperglycemia so that energy is readily available at the repair site.

Among many, many other things, the authors of this paper found that administering insulin to burned rats stabilized gastric motility and increased clearance. Introducing insulin into the system would clear glucose out of the blood and put it back into storage in the body, reducing hyperglycemia in the rats. The authors theorize that insulin also acts to potentiate the effects of stronger vasodilators like nitric oxide, which would then increase the blood flow to the gastrointestinal tract.

What does this mean for the patient? As I've mentioned, rebuilding issue is metabolically expensive, and recovering patients have high energy demands that often can't be met because eating is ineffective due to the symptoms outlined above. Patients may experience uncomfortable GI side effects such as ulcerations, bleeding, vomiting, and distention. Increasing gut motility and clearance by treatment with insulin after a severe cutaneous burn may ameliorate some of these symptoms and provide the patient with more energy for the healing process than would be available via other routes of administration.

However, I can't help wondering what effect this may have on healing. Do the energetic benefits of enteral feeding outweigh the energetic costs of running the GI tract at normal speed? And by not forcing the body to run on ketones, would it be more likely that pathogens could enter the body at a time when the immune system is compromised because most of the body's resources are being shunted towards repair? Unfortunately this study doesn't answer any of those questions, since the rats had to be killed in order to measure gastric clearance. I would like to see a future study that examines the treatments administered here and their effects on the healing process.

EDIT: The more I think about this paper, the more I wonder how dehydration is factoring into the equation. After a serious burn, often the skin permeability barrier is compromised, and patients lose water via evaporation rapidly through the wound. As a result, burn patients can quickly become dehydrated. I searched the methods to see if the authors were accounting for this, and I saw no evidence that they were. All they mention is that "[B]lood glucose level was measured preburn, 6 h after burn and 30 min after meal, using a commercially available glucometer." If the authors are not counting for dehydration and possible loss in blood volume because of that, the blood glucose level could appear to be higher when in fact the animal had a normal total amount of glucose in their blood.

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Sallam, H., Oliveira, H., Liu, S., & Chen, J. (2010). Mechanisms of Burn-induced Impairment in Gastric Slow Waves and Emptying in Rats AJP: Regulatory, Integrative and Comparative Physiology DOI: 10.1152/ajpregu.00135.2010