Postnatal monosodium glutamate treatment results in attenuation of corticosterone metabolic rate in adult rats.
OBJECTIVE
To study the basal and ACTH stimulated production of corticosterone by adrenal cortex on one hand and the binding and degradation of corticosterone in the liver of adult rats which were treated with monosodium glutamate (MSG) during the neonatal period.


METHODS
Male offsprings of Sprague-Dawley rats were injected i.p. with MSG (4 mg/g of b.w. in saline) on alternated days for the first 10 days of life, their littermates being used as controls. On the 21st postnatal day they were weaned and used for the observation at the age of 65-75 days. After sacrifice the level of corticosterone in serum and the release of corticosterone from incubated adrenals under basal and ACTH stimulated conditions (ACTH in 6 concentrations from 1.25 to 80 mU/ml medium) were estimated. In addition, glucocorticoid binding to cytosol receptors in the liver and muscle tissues was determined. Corticosterone degradation rate was measured by decrease of corticosterone concentration added to the medium after the incubation with liver slices.


RESULTS
Adult rats neonatally treated with MSG had reduced weight of adrenal glands, while plasma corticosterone levels and its basal production by adrenals in vitro were significantly higher than in controls. In MSG treated rats the stimulation of corticosterone production by ACTH was diminished. Glucocorticoid binding to liver cytosolic receptors was significantly decreased, while that in muscle tissue was only slightly elevated. Moreover, a decreased corticosterone degradation rate in liver slices was observed in rats treated neonatally with MSG.


CONCLUSIONS
These results are in agreement with previously observed decrease of corticosterone clearance rate in MSG treated animals and suggest that elevated corticosterone levels in plasma and its prolonged response to stressogenic stimulation are due to elevated corticosterone production in adrenals and lower degradation rate in the liver.
Macho
L
L
Institute of Experimental Endocrinology, Slovak Academy of Sciences, 83306 Bratislava, Slovakia. ueenmacho@savba.savba.sk
Jezova
D
D
Zorad
S
S
Fickova
M
M
D000302:Adrenal Cortex / Q000187:drug effects / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D001481:Basal Metabolism; D001835:Body Weight / Q000187:drug effects; D003345:Corticosterone / Q000378:metabolism*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012970:Sodium Glutamate / Q000627:therapeutic use*; D013268:Stimulation, Chemical
D000324:Adrenocorticotropic Hormone; D012970:Sodium Glutamate; D003345:Corticosterone