OBJECTIVE: To study the pattern of the alterations of blood glucose, insulin and insulin sensitivity after traumatic brain injury in rats, and verify the occurrence of insulin resistance after the injury. METHODS: Based on Feeney's model of brain injury, the blood glucose and insulin concentration of the dogs measured 30 min before and at 6, 12, 24, 48, 72 and 120 h after injury. BG60-120, GIR60-120, and insulin sensitivity index (ISI) reflecting the insulin sensitivity were measured at 6, 24, 48, and 72 hours following severe traumatic brain injury using euglycemic-hyperinsulinemic clamp. RESULTS: Both the blood glucose and insulin concentration increased markedly in rats following moderate and severe brain injury. BG60-120 increased markedly, and GIR60-120 and ISI decreased significantly 6, 24, 48, and 72 h after severe brain trauma as compared with those of the sham operation group. Blood glucose concentration of rats following severe injury was positively correlated with insulin concentration and BG60-120 at the corresponding time points, but negatively with GIR60-120 and ISI. CONCLUSION: Both the blood glucose and insulin concentration increase markedly in rats following severe brain injury. Increased blood glucose even in the presence of high-level insulin is due to acute insulin resistance occurring after traumatic brain injury.
OBJECTIVE: To study the pattern of the alterations of blood glucose, insulin and insulin sensitivity after traumatic brain injury in rats, and verify the occurrence of insulin resistance after the injury. METHODS: Based on Feeney's model of brain injury, the blood glucose and insulin concentration of the dogs measured 30 min before and at 6, 12, 24, 48, 72 and 120 h after injury. BG60-120, GIR60-120, and insulin sensitivity index (ISI) reflecting the insulin sensitivity were measured at 6, 24, 48, and 72 hours following severe traumatic brain injury using euglycemic-hyperinsulinemic clamp. RESULTS: Both the blood glucose and insulin concentration increased markedly in rats following moderate and severe brain injury. BG60-120 increased markedly, and GIR60-120 and ISI decreased significantly 6, 24, 48, and 72 h after severe brain trauma as compared with those of the sham operation group. Blood glucose concentration of rats following severe injury was positively correlated with insulin concentration and BG60-120 at the corresponding time points, but negatively with GIR60-120 and ISI. CONCLUSION: Both the blood glucose and insulin concentration increase markedly in rats following severe brain injury. Increased blood glucose even in the presence of high-level insulin is due to acute insulin resistance occurring after traumatic brain injury.