Based on the measurements in our burn patients, burn injury triggers
a two-fold increase (20 kcal/kg/day) in resting energy expenditure
(REE) of our patients. Compared to other processes such as sepsis,
peritonitis, skeletal trauma and elective surgery, this increase in
REE from burn injury is the most dramatic. However, one should remain
optimistic that this severe, damaging phenotype can be controlled,
since the overall magnitude of this response appears to have diminished
since the 1970s and this is likely, at least in part, to be related
to improvements in modern comprehensive burn care.
In addition to the hypermetabolic increase in REE, a more problematic
metabolic feature is self-catabolism, or wasting of muscle tissue,
which routinely follows a burn injury, and this catabolic response
is presumably a consequence of the increase in REE or is related
to it. The self-catabolism, which is manifested by a two-fold increase
in protein degradation with a lesser increase in synthesis, persists
despite state-of-the-art nutritional care. As a result, the rate
of protein degradation continues to exceed that of synthesis by
1.3 g/kg/day in our patients. The driver(s) for the catabolic, hypermetabolic
response, which are considered below, remain fundamentally unknown.
Manipulation of the Hypermetabolic Response
Unfortunately,
there has been very limited success to directly attenuate this catabolic,
hypermetabolic response thus far. Anabolic hormones (rhGH, IGF-1/bp
3, insulin, testosterone, and oxandrolone) promised to raise the
rate of protein synthesis while lowering the rate of net protein
loss. These agents however do not appear to affect the rate of protein
degradation, although they do increase protein synthesis substantially.
Therefore, the net effect of these agents only serves to potentially
increase REE. Similarly, the inhibition of cytokines has not favorably
influenced the catabolic, hypermetabolic response. On the other
hand, propranolol, which is a nonspecific beta-blocker, has been
successful, at least in part. Although the overall metabolic rate
has been decreased with propranolol, it is not likely to be adopted
as standard treatment in modern burn care because of its broad and
nonspecific effects on the cardiovascular and metabolic systems.
Therefore, broadly interpreted, our Center research focuses on key
amino acids in their role to regulate protein synthesis and degradation
and on insulin receptor function.
Unfortunately,
there has been very limited success to directly attenuate this catabolic,
hypermetabolic response thus far. Anabolic hormones (rhGH, IGF-1/bp
3, insulin, testosterone, and oxandrolone) promised to raise the
rate of protein synthesis while lowering the rate of net protein
loss. These agents however do not appear to affect the rate of protein
degradation, although they do increase protein synthesis substantially.
Therefore, the net effect of these agents only serves to potentially
increase REE. Similarly, the inhibition of cytokines has not favorably
influenced the catabolic, hypermetabolic response. On the other
hand, propranolol, which is a nonspecific beta-blocker, has been
successful, at least in part. Although the overall metabolic rate
has been decreased with propranolol, it is not likely to be adopted
as standard treatment in modern burn care because of its broad and
nonspecific effects on the cardiovascular and metabolic systems.
Therefore, broadly interpreted, our Center research focuses on key
amino acids in their role to regulate protein synthesis and degradation
and on insulin receptor function.