glucagon-like-peptide-1 and Burns

Although glucagon-like peptide 1 levels have been closely associated with inflammation and mortality in septic patients, the clinical importance of glucagon-like peptide 1 on hospital-acquired infections and long-term mortality after burn injury remains unexplored.. Plasma samples from 144 burn patients were collected on admission to determine total glucagon-like peptide 1, interleukin 6, and monocyte chemotactic protein-1 levels. Hospital-acquired infections were determined by positive microbial culture. One-year mortality was assessed by telephone interview. Factors associated with glucagon-like peptide 1 were determined by multivariable linear logistic regression. Predicting the clinical importance of glucagon-like peptide 1 on the development of hospital-acquired infections and mortality were determined by Cox proportional hazards models and further by receiver operating characteristic curve analysis. Kaplan-Meier analyses were performed to examine whether the mean glucagon-like peptide 1 level of the cohort could discriminate the hospital-acquired infections-free survival.. Median burn size was 41% (19%-70%) of total body surface area. Hospital-acquired infections developed in 36 (25%) patients after a mean of 10 ± 1 days after injury. Interleukin 6, monocyte chemotactic protein-1, and blood urea nitrogen levels and thrombin time were independently associated with increased glucagon-like peptide 1 levels. Levels of glucagon-like peptide 1 (median, interquartile range) were greater in patients who developed hospital-acquired infections than in those who did not (237 pmol/L, 76-524 vs 80 pmol/L, 51-158; P < .001) and in patients who died (536 pmol/L, interquartile range: 336-891 pmol vs 98 pmol/L, 47-189; P < .001). Although the glucagon-like peptide 1 level could not predict hospital-acquired infections-free survival in individual patients, it could predict 1-year mortality independently (P = .021). Moreover, a glucagon-like peptide 1 level of 200 pmol/L could discriminate hospital-acquired infections-free survival (P < .001).. Admission glucagon-like peptide 1 level can discriminate hospital-acquired infections-free survival and predict long-term mortality in a group of patients with burn injury. Our data suggests that glucagon-like peptide 1 may be a predictive biomarker for hospital-acquired infections and mortality in burn patients.

Topics: Adult; Biomarkers; Blood Urea Nitrogen; Burns; Chemokine CCL2; Cross Infection; Female; Glucagon-Like Peptide 1; Humans; Injury Severity Score; Interleukin-6; Male; Middle Aged; Retrospective Studies; Thrombin Time

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.

Topics: Alcoholic Intoxication; Animals; Blood Glucose; Burns; Ethanol; Gastric Inhibitory Polypeptide; Ghrelin; Glucagon-Like Peptide 1; Insulin; Leptin; Mice, Inbred C57BL; Models, Animal; Plasminogen Activator Inhibitor 1; Resistin

Hyperglycemia with insulin resistance is commonly seen in severely burned patients and tight glycemia control with insulin may be beneficial in this condition. The most potent insulinotropic hormone, glucagon-like peptide 1 (GLP-1), stimulates insulin secretion in a glucose-dependent manner. Because infusion of GLP-1 never reduces glucose levels to below ∼70 mg/dL, the risk of hypoglycemia by using insulin is reduced. In this study we investigated the metabolic effects of GLP-1 infusion after burn injury in an animal model.. Male CD rats were divided in 3 groups: burn injury with saline, burn injury with GLP-1 treatment, and sham burn (SB). Burn injury was full thickness 40% total body surface area. The burn injury with GLP-1 treatment group received GLP-1 infusion via osmotic pump. Fasting blood glucose, plasma insulin, and plasma GLP-1 levels were measured during intraperitoneal glucose tolerance tests. Expressions of caspase 3 and bcl-2 were evaluated in pancreatic islets. In a subset of animals, protein metabolism and total energy expenditure were measured.. Fasting GLP-1 was reduced in burn injury with saline compared to SB or burn injury with GLP-1 treatment. Burn injury with GLP-1 treatment showed reduced fasting blood glucose, improved intraperitoneal glucose tolerance test results, with increased plasma insulin and GLP-1 responses to glucose. GLP-1 reduced protein breakdown and total energy expenditure in burn injury with GLP-1 treatment versus burn injury with saline, with improved protein balance. Increased expression of caspase 3 and decreased expression of bcl-2 in islet cells by burn injury were ameliorated by GLP-1.. Burn injury reduced plasma GLP-1 in association with insulin resistance. GLP-1 infusion improved glucose tolerance and showed anabolic effects on protein metabolism and reduced total energy expenditure after burn injury, possibly via insulinotropic and non insulinotropic mechanisms.

Topics: Animals; Blood Glucose; Burns; Caspase 3; Energy Metabolism; Glucagon-Like Peptide 1; Hyperglycemia; Incretins; Insulin; Insulin Resistance; Islets of Langerhans; Male; Models, Animal; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Inbred Strains