Idrovo Juan-Pablo, Shults Jill A, Curtis Brenda J, Chen Michael M, Kovacs Elizabeth J
Division of GI, Trauma and Endocrine Surgery, Department of Surgery, Burn Research and Alcohol Research Programs, University of Colorado, Denver, Aurora, Colorado.
Department of Surgery, Alcohol Research Program, Loyola University Chicago, Maywood, Illinois.
J Burn Care Res. 2019 Oct 16;40(6):785-791. doi: 10.1093/jbcr/irz083.
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.
胃肠激素在烧伤后代谢中至关重要。由于近50%的烧伤患者在入院时血液酒精水平检测呈阳性,且与未中毒的烧伤患者相比预后较差;我们推测中毒的烧伤患者胃肠激素分泌受损。为了验证我们的理论,我们在乙醇中毒和烧伤联合损伤的小鼠模型中对胃肠激素血清水平进行了量化。因此,小鼠连续3天每日给予乙醇剂量,休息4天,然后再额外给予乙醇3天。在最后一次给予乙醇剂量30分钟后,小鼠接受15%体表面积的烫伤。在烧伤损伤后24小时收集血清样本。与假手术对照组小鼠相比,未中毒的烧伤小鼠的葡萄糖、胰岛素、胃饥饿素、纤溶酶原激活物抑制剂-1、瘦素和抵抗素分别增加了1.4倍、3倍、13.5倍、6.2倍、9.4倍和2.4倍(P < 0.05)。与假手术损伤、给予赋形剂处理的小鼠相比,烧伤损伤还使血清胃抑制多肽(GIP)降低了32%。当烧伤损伤前发生中毒时,瘦素、抵抗素、胰高血糖素样肽-1以及胰岛素与假手术组无差异。然而,在用乙醇处理的烧伤小鼠中,胃抑制多肽和胰高血糖素血清水平分别显著增加了3.5倍和4.7倍。根据这些结果,我们得出结论,烧伤损伤后24小时,小鼠胃肠激素出现显著变化,同时伴有高血糖。此外,烧伤和乙醇中毒的联合损伤导致了额外的激素变化,这可能归因于潜在的胰腺功能障碍。需要进一步进行多日研究以探讨这些激素变化的病因、行为和临床意义。