Early hormonal changes affect the catabolic response to trauma.
OBJECTIVE
The authors sought to determine how temporary insulin suppression might alter the catabolic effects of cortisol, glucagon, and epinephrine.


BACKGROUND
The metabolic responses to injury include hypermetabolism, accelerated net skeletal muscle protein breakdown, glucose intolerance, and insulin resistance. These alterations are associated with increased stress hormone concentrations. Insulin elaboration is usually suppressed immediately after an injury but is abundant later during convalescence. An infusion of hydrocortisone, glucagon, and epinephrine increases both stress hormone concentrations and insulin levels. It induces many of the metabolic alterations seen in critically ill patients, but it does not affect net muscle breakdown.


METHODS
Seven healthy adults received a stress hormone infusion for 3 days in two separate studies. During one study they, also received an infusion of the somatostatin analogue, octreotide (0.005 micrograms/kg/min), to suppress insulin elaboration for the first 24 hours. During the other study (control), insulin was permitted to rise unchecked.


RESULTS
Stress hormone concentrations, hypermetabolism (+/- 20% above basal), and leukocytosis were similar during both study periods. When insulin elaboration was temporarily suppressed, whole-body nitrogen loss was increased during the first 48 hours, and the efflux of amino acids from the forearm after 72 hours of infusion was 60% greater than the control level.


CONCLUSIONS
Temporary insulin suppression during physiologic increases in stress hormone concentrations amplified whole-body nitrogen loss and led to the development of accelerated net skeletal muscle protein breakdown. Early hormonal changes after an injury may affect the development of later catabolic responses.
Bessey
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PQ
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri.
Lowe
K A
KA
D000328:Adult; D000596:Amino Acids / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism*; D002151:Calorimetry; D004837:Epinephrine / Q000378:metabolism*; D005260:Female; D005934:Glucagon / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009584:Nitrogen / Q000378:metabolism; D015282:Octreotide / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014947:Wounds and Injuries / Q000378:metabolism*
D000596:Amino Acids; D001786:Blood Glucose; D007328:Insulin; D007773:Lactates; D019344:Lactic Acid; D005934:Glucagon; D012964:Sodium; D009584:Nitrogen; D015282:Octreotide; D011188:Potassium; D006854:Hydrocortisone; D004837:Epinephrine