Section V: METABOLIC RESPONSE TO STARVATION

In the non-stressed starved patient, decreased nutrient intake leads to a decrease in metabolic activity, thereby conserving energy.  A severe decrease in nutrient intake leads to a rapid depletion of the body’s carbohydrate stores.  This process would be found in elective surgery patients made NPO prior to the procedure.  In addition, patients may arrive with a pre-existing semi-starved state.  After surgery or trauma the “stress response” takes over and over-rides the adaptive starvation response.

Because key tissues such as the brain are obligate users of carbohydrate, gluconeogenesis in the liver must provide the necessary carbohydrate.  The initial substrate for new carbohydrate formation are the amino acids resulting from muscle breakdown.  An additional mechanism to provide substrate is via incomplete glucose metabolism to lactate in tissues, with recycling of lactate to the liver for carbohydrate formation via the Cori cycle.  In the absence of increased levels of insulin as a result of low carbohydrate levels, lipolysis can occur, with the production of ketone bodies for subsequent use as calories.  This process of ketosis is inhibited in stress states, in the presence of high levels of catechols and corticoids.  Obligate carbohydrate users such as the brain and red cells require some glucose but most other tissues can effectively utilize ketone bodies for energy.  Ketosis and ketonuria (acetone) are evidence of this process and characteristic of the semi-starved state.  This response is an adaptive one that preserves lean body mass and decreases energy demands.