ABSTRACT
In prolonged critical illness (vital organ function supported with intensive care for weeks), feeding is unable to reverse ongoing wasting of protein, whereas fat is preserved or even further stored (1,2). This feeding-resistant loss of protein is mainly caused by its activated degradation together with suppressed synthesis; thereby, dramatically reducing the protein content of vital tissues. The residual protein content in skeletal muscle of critically ill patients apparently correlates inversely with the duration, instead of the severity, of illness, and is mainly determined by the (impaired) capacity to synthesize protein (2). The mechanisms underlying these inappropriate metabolic responses in the fed, critically ill state remain incompletely understood.
