Insulin protects against hepatic damage postburn.

Area of Science:

• Biomedical science
• Physiology
• Injury research

Background:

• Burn injuries cause significant liver dysfunction, characterized by endoplasmic reticulum (ER) stress and the unfolded protein response (UPR).
• ER stress/UPR pathways contribute to liver cell death (apoptosis) and metabolic disruptions following burns.
• Insulin is known to mitigate hepatic damage and enhance liver function.

Purpose of the Study:

• To investigate the hypothesis that insulin administration attenuates post-burn hepatic ER stress and subsequent apoptosis.
• To evaluate the protective effects of insulin on liver structure and function after severe burn injury.

Main Methods:

• Male Sprague Dawley rats underwent a 60% total body surface area (TBSA) burn injury.
• Animals received either saline (control) or insulin (2.5 IU/kg q. 24 h) and were euthanized at 24 and 48 hours postburn.
• Liver structure, function, ER stress markers, apoptosis, mitochondrial integrity, and inflammatory mediators were assessed.

Main Results:

• Burn injury induced ER stress, mitochondrial dysfunction, hepatocyte apoptosis, and inflammation.
• Insulin treatment significantly decreased hepatocyte apoptosis and caspase-3 activation at both 24 and 48 hours postburn.
• Insulin administration reduced ER stress, improved mitochondrial structure and function, and attenuated inflammatory mediator expression (IL-6, MCP-1, CINC-1).

Conclusions:

• Insulin therapy effectively alleviates burn-induced endoplasmic reticulum stress, hepatocyte apoptosis, mitochondrial abnormalities, and inflammation.
• These findings demonstrate that insulin improves hepatic structure and function post-burn.
• Insulin therapy shows promise for improving patient outcomes after traumatic injuries.