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The effect of leucine on plasma insulin following endotoxin shock in the rat
We have previously documented the ability of exogenous L-leucine to accelerate the endotoxin shock syndrome. In this report we have tested the hypothesis that the mechanism for this action of leucine was via an induction of pancreatic insulin hypersecretion. Pentobarbital-anesthetized rats were injected with 1 mg/100 gm S. enteritidis endotoxin (LD90) or vehicle and infused with either Krebs Henseleit vehicle or 0.153 M leucine to a dose of 7.6 mmole/kg. Following leucine administration, plasma concentrations of leucine decayed at an exponential rate in both endotoxin-treated and sham-treated groups. The extrapolated initial leucine concentration in the endotoxin-treated rats was significantly higher than the sham rats, indicating a lower circulating blood volume in the endotoxin-treated group. In the vehicle and endotoxin-treated group, insulin levels exhibited a biphasic response, significantly lower at 30 minutes and significantly higher at three hours. In the leucine- and endotoxin-treated groups, insulin levels were markedly higher 0.5, 2, and 3 hours after leucine infusion. In the two non-endotoxin treated groups, no significant changes in insulin levels were noted after infusion. Therefore, the shock accelerating action of leucine may be due to a direct stimulation of insulin secretion inducing a prolonged hyperinsulinemia.
We have previously documented the ability of exogenous L-leucine to accelerate the endotoxin shock syndrome. In this report we have tested the hypothesis that the mechanism for this action of leucine was via an induction of pancreatic insulin hypersecretion. Pentobarbital-anesthetized rats were injected with 1 mg/100 gm S. enteritidis endotoxin (LD90) or vehicle and infused with either Krebs Henseleit vehicle or 0.153 M leucine to a dose of 7.6 mmole/kg. Following leucine administration, plasma concentrations of leucine decayed at an exponential rate in both endotoxin-treated and sham-treated groups. The extrapolated initial leucine concentration in the endotoxin-treated rats was significantly higher than the sham rats, indicating a lower circulating blood volume in the endotoxin-treated group. In the vehicle and endotoxin-treated group, insulin levels exhibited a biphasic response, significantly lower at 30 minutes and significantly higher at three hours. In the leucine- and endotoxin-treated groups, insulin levels were markedly higher 0.5, 2, and 3 hours after leucine infusion. In the two non-endotoxin treated groups, no significant changes in insulin levels were noted after infusion. Therefore, the shock accelerating action of leucine may be due to a direct stimulation of insulin secretion inducing a prolonged hyperinsulinemia.