Abstract
Sepsis alters the dynamic flux of metabolic substrates between skeletal muscle and liver. Derangements in skeletal muscle glucose metabolism evoked by sepsis to a certain extent determine the rate of gluconeogenesis in the liver. In contrast, accelerated rates of gluconeogenesis do not drive net catabolism in skeletal muscle, nor does the upregulation of hepatic protein metabolism in sepsis or inflammation appear to be contingent or dependent upon the catabolism of muscle proteins during sepsis.