INSULIN TO INHIBIT PROTEIN CATABOLISM AFTER INJURY

Using patients with varying degrees of trauma as their own controls we compared three isocaloric regimens in three-day crossover studies; 9.4 g of nitrogen as l-amino acids was also given daily. The urea production rate was used as an index of protein breakdown. We found that in catabolic patients, insulin and glucose produced a strikingly greater inhibition of protein breakdown than glucose alone, and that glucose alone was marginally more protein sparing than a regimen containing mainly fat (Intralipid and sorbitol). These differences were not seen in non-catabolic patients (urea production rate <15 g daily). In the catabolic patients (urea production rate >15 g daily) the protein-sparing effect of insulin was proportional to the initial urea production rate. We therefore concluded that insulin has important protein-sparing effects in severely ill traumatized patients, but little effect when there is no increased catabolic rate. (N Engl J Med 300:14–17, 1979) DURING starvation, the body draws upon its fat stores to meet energy requirements and upon muscle protein for both gluconeogenesis and labile protein reserves. A decrease in metabolic rate and adaptation of the central nervous system to the oxidation of ketones as well as glucose allows a fall in the rate of gluconeogenesis and preservation of protein stores.1 In contrast, after injury, there is an increase in metabolic rate and protein breakdown that is proportional to the severity of injury and lasts as long as the illness and its complications persist.2,3 Kinney et al.4 showed that, after injury, energy is. © 1979, Massachusetts Medical Society. All rights reserved.