Background
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, gucagon-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.
Methods
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.
Results
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.
Conclusion
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.
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Article info
Publication history
Published online: February 07, 2011
Accepted:
November 24,
2010
Footnotes
Supported by the National Institutes of Health (2P50 GM 021700 GM 07035) and Shriners Hospitals for Children (Grant 8470).
Identification
Copyright
© 2011 Mosby, Inc. Published by Elsevier Inc. All rights reserved.