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Updated: Aug 5, 2026

Pseudofracture: An Acute Peripheral Tissue Trauma Model
Published on: April 18, 2011
Insulin and trauma: some thoughts
1Howard Hughes Medical Institute, 398 Brookline Avenue, Boston, Massachusetts 02215, USA.
Trauma and/or sepsis produce a net negative nitrogen balance due mainly to muscle protein breakdown. Lymphokines (interleukins) appear to be the hormonal signal which negates insulin's anabolic effect on muscle resulting in net catabolism. In contrast, their effects on immune and reparative cells appear additive to insulin's anabolic effect augmenting tissue repair and increasing immunologic defense, but at the expense of muscle nitrogen. This logical evolutionary adaptation did not anticipate that parenteral alimentation could provide both the needed glucose for tissue repair, thus obviating muscle protein catabolism to provide precursor amino acids for hepatic gluconeogenesis and the amino acids for tissue reconstruction.
Trauma and/or sepsis produce a net negative nitrogen balance due mainly to muscle protein breakdown. Lymphokines (interleukins) appear to be the hormonal signal which negates insulin's anabolic effect on muscle resulting in net catabolism. In contrast, their effects on immune and reparative cells appear additive to insulin's anabolic effect augmenting tissue repair and increasing immunologic defense, but at the expense of muscle nitrogen. This logical evolutionary adaptation did not anticipate that parenteral alimentation could provide both the needed glucose for tissue repair, thus obviating muscle protein catabolism to provide precursor amino acids for hepatic gluconeogenesis and the amino acids for tissue reconstruction.
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