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Alcohol Intoxication and the Postburn Gastrointestinal Hormonal Response
Author(s) -
Juan-Pablo Idrovo,
Jill A. Shults,
Brenda J. Curtis,
Michael M. Chen,
Elizabeth J. Kovacs
Publication year - 2019
Publication title -
journal of burn care and research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.679
H-Index - 78
eISSN - 1559-0488
pISSN - 1559-047X
DOI - 10.1093/jbcr/irz083
Subject(s) - medicine , burn injury , hormone , ghrelin , endocrinology , resistin , glucagon , alcohol intoxication , leptin , insulin , peptide hormone , pancreatic polypeptide , adiponectin , poison control , insulin resistance , surgery , environmental health , injury prevention , obesity
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.

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