Alcohol Intoxication and the Postburn Gastrointestinal Hormonal Response

Abstract

Gastrointestinal hormones are essential in postburn metabolism. Since near 50% of burn victims test positive for blood alcohol levels at hospital admission and have inferior outcomes compared to nonintoxicated burn patients; we hypothesized that the gastrointestinal hormone secretion is compromised in intoxicated burn victims. To test our theory, we quantified gastrointestinal hormones serum levels in a combine ethanol intoxication and burn injury mouse model. Thus, mice received a daily dose of ethanol for 3 days, rested 4 days, and were given ethanol 3 additional days. Mice underwent 15% TBSA scald burn 30 minutes after their last ethanol dose. Serum samples were collected 24 hours after burn injury. Nonintoxicated burned mice exhibited an increase in glucose, insulin, ghrelin, plasminogen activator inhibitor-1, leptin, and resistin by 1.4-, 3-, 13.5-, 6.2-, 9.4-, and 2.4-fold, respectively, compared to sham vehicle mice (P < .05). Burn injury also reduced serum gastric inhibitory polypeptide (GIP) by 32% compared to sham-injured, vehicle-treated mice. Leptin, resistin, glucagon-like peptide-1, as well as insulin, were not different from sham groups when intoxication preceded burn injury. Nevertheless, in burned mice treated with ethanol, gastric inhibitory polypeptide and glucagon serum levels exhibited a significant fold increase of 3.5 and 4.7, respectively. With these results, we conclude that 24 hours after burn injury, mice developed significant changes in gastrointestinal hormones, along with hyperglycemia. Moreover, the combined insult of burn and ethanol intoxication led to additional hormonal changes that may be attributed to a potential pancreatic dysfunction. Further multiday studies are required to investigate the etiology, behavior, and clinical significance of these hormonal changes.

Morphofunctional State and Circadian Rhythms of the Liver under the Influence of Chronic Alcohol Intoxication and Constant Lighting

“…Thus, the hyperglycemia we found in animals of the first and second experimental groups is explained in the first case by the well-known effect of CAI, which can cause disorders of carbohydrate metabolism, manifesting in both hyper- (more often) and in hypoglycemia [ 68 , 69 ], and in the second case by a response to stressful effects. At the same time, a significant decrease in the levels of this metabolite in the blood plasma of rats of the third group was caused by a disruption of the adaptation process.…”

Integrated analysis of dysregulated microRNA and mRNA expression in intestinal epithelial cells following ethanol intoxication and burn injury

“…Although both burn injury and chronic alcohol consumption promote hypermetabolism, there are few studies which explore the impact of combined alcohol intoxication and burn injury on metabolic outcomes. One recent study revealed significant alterations in metabolism after combined insult, including hyperglycemia and changes in serum insulin, glucagon and gastrointestinal hormones in alcohol and burn mice compared to sham or burn alone 35 . In our study, almost all KEGG pathways significantly associated with upregulated genes in IECs after alcohol and burn injury were metabolic in nature (Fig.…”

Integrated Analysis of Dysregulated microRNA and mRNA Expression in Intestinal Epithelial Cells following Ethanol Intoxication and Burn Injury

“…Although both burn injury and chronic alcohol consumption promote hypermetabolism, there are few studies which explore the impact of combined alcohol intoxication and burn injury on metabolic outcomes. One recent study revealed signi cant alterations in metabolism after combined insult, including hyperglycemia and changes in serum insulin, glucagon and gastrointestinal hormones in alcohol and burn mice compared to sham or burn alone 35 . In our study, almost all KEGG pathways signi cantly associated with upregulated genes in IECs after alcohol and burn injury were metabolic in nature (Fig.…”