Acute (i.e., wasting) pediatric
malnutrition consistently elevates blood
glucocorticoid levels, but neither the magnitude of the rise in concentration nor its kinetics is clear. Male and female C57BL/6J mice, initially 19 days old, and CBA/J mice, initially 23 days old, consumed a complete purified diet either ad libitum (age-matched control) or in restricted daily quantities (mimicking
marasmus), or they consumed a purified isocaloric
low-protein diet ad libitum (mimicking incipient
kwashiorkor). Serum levels of
corticosterone were assessed by double antibody radioimmunoassay after 3, 6, and 14 days (C57BL/6J strain) or after 6 and 14 days in the genetically distant CBA/J strain. Age-matched control groups of both strains exhibited mean
corticosterone levels of 5-30 ng/ml, whereas the acutely malnourished groups exhibited mean levels of this
hormone that were elevated by more than an order of magnitude as early as 3 days after initiation of
weight loss. This outcome was confirmed in a second experiment in which the serum
corticosterone level of C57BL/6J weanlings was examined by competitive binding
enzyme immunoassay 3 and 14 days after initiation of the dietary protocols. Therefore, deficits of
protein and/or energy in weanling murine systems relevant to acute pediatric
malnutrition elicit early elevations in blood
glucocorticoid levels to a magnitude reminiscent of
critical illness and
multiple trauma. The key to this novel finding was an
exsanguination method that permitted accurate assessment of the blood
corticosterone level of the healthy, quiescent mouse. Overall, the results of this investigation provide a new perspective on the
glucocorticoids as part of the early hormonal response to acute weanling
malnutrition coincident with the shift toward catabolic metabolism and the initiation of depression in cellular immune competence.