Metabolic Changes in Sepsis

Nutrition for Special Groups 3(3+0)

Lesson 45 : Sepsis

Metabolic Changes in Sepsis

Skeletal Muscle Protein Metabolism

In addition to its role in locomotion, skeletal muscle (by virtue of its mass in relationship to body weight) represents the major reservoir of amino acids. Some of these amino acids, including alanine, serine, and glycine, are important substrates for gluconeogenesis in liver and kidney. Protein wasting is a general feature of trauma, sepsis, and burns. The earliest recognizable disturbance in protein metabolism in the injury process is excessive urea excretion, resulting in a loss of nitrogen from the body.
Sepsis caused a decrease in the muscle weight of all four muscles.

The increased rate of net catabolism in sepsis can result from a rise in protein degradation, or a decrease in protein synthesis, or both. The relative importance of protein synthesis versus degradation in the induction of the negative nitrogen balance during sepsis is unresolved. The increased net catabolism after trauma uncomplicated by sepsis results from an inhibition of protein synthesis rather than a change in protein degradation.

Insulin Resistance in Sepsis

In the case of sepsis, insulin resistance is manifested by either an abnormal glucose tolerance test or simply an elevated plasma glucose concentration for a given insulin concentration. This insulin resistance could occur by alterations at one of three levels: (1) before the interaction of insulin with the receptor, (2) at the receptor level, or (3) at steps distal to the insulin-receptor interaction, namely, cellular metabolism. Insulin concentration is the same or increased in sepsis, and no anti-insulin antibodies have been detected. At the receptor level, the sensitivity of the receptor to circulating insulin appears to be normal. Hence, it appears that insulin resistance in sepsis may be related to an intracellular defect in glucose metabolism.

Last modified: Friday, 11 May 2012, 5:22 AM