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Related Experiment Videos

Carbohydrate dynamics in the hypermetabolic septic rat.

C H Lang, G J Bagby, J J Spitzer

    Metabolism: Clinical and Experimental
    |October 1, 1984
    PubMed
    Summary

    Sepsis significantly increases glucose turnover and clearance by enhancing gluconeogenesis, not glycogenolysis. Lactate becomes a key precursor, and hormonal changes favor glucose production.

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    Area of Science:

    • Metabolic regulation during sepsis
    • Carbohydrate metabolism in critical illness

    Background:

    • Sepsis induces a hypermetabolic state, increasing glucose turnover.
    • Regulation of carbohydrate metabolism during sepsis remains incompletely understood.

    Purpose of the Study:

    • To investigate glucose and lactate kinetics during the hypermetabolic phase of sepsis.
    • To determine the contribution of glycogenolysis and gluconeogenesis to glucose production in sepsis.

    Main Methods:

    • Peritoneal sepsis induced in rats via fecal inoculum.
    • Chronic vascular catheterization for tracer infusion.
    • Constant infusion of radiolabeled tracers to study glucose and lactate kinetics on day 2 of sepsis.

    Main Results:

    • Septic rats showed a 42% increase in glucose turnover and 63% increase in glucose metabolic clearance rate.
    • Hepatic glycogenolysis contributed minimally (1-2%) to glucose appearance.
    • Glucose recycling increased by 93%, indicating enhanced gluconeogenesis.
    • Lactate turnover increased by 34%, with increased conversion of glucose to lactate.
    • Insulin levels decreased by 56%, glucagon increased by 67%, lowering the insulin/glucagon ratio.

    Conclusions:

    • Increased peripheral glucose uptake in sepsis generates more gluconeogenic precursors.
    • Gluconeogenesis, particularly from lactate, is a major contributor to elevated glucose turnover.
    • Hepatic glycogenolysis plays a minor role in glucose production during hypermetabolic sepsis.
    • Hormonal changes (decreased insulin, increased glucagon) support glucose production in sepsis.

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