Protection from lethal endotoxic shock after testosterone depletion is linked to chromosome X.

Men are considered more susceptible to sepsis after severe injury than are women, which has been attributed to a suppressing effect of male sex steroids on the inflammatory response. Moreover, the effect of sex steroids on the inflammatory process depends on the genetic background. The present study examined the genetic contribution to survival after endotoxic shock in mice depleted of testosterone by surgical castration.

Accelerated recovery after endotoxic challenge in heat shock-pretreated mice.

The inflammatory response induced by bacterial lipopolysaccharide (LPS) has profound metabolic and physiological effects. Thus hepatic glucose production is depressed after LPS administration, which is, at least in part, due to the downregulation of phosphoenolpyruvate carboxykinase (PEPCK) expression. PEPCK is a key regulatory enzyme of the gluconeogenic pathway.