The mechanisms underlying the onset of obesity are complex and not completely 
understood. An imbalance of autonomic nervous system has been proposed to be a 
major cause of great fat deposits accumulation in hypothalamic obesity models. 
In this work we therefore investigated the adrenal chromaffin cells in 
monosodium glutamate (MSG)-treated obese female mice. Newborn mice were injected 
daily with MSG (4 mg/g body weight) or saline (controls) during the first five 
days of life and studied at 90 days of age. The adrenal catecholamine content 
was 56.0% lower in the obese group when compared to lean controls (P < 0.0001). 
Using isolated adrenal medulla we observed no difference in basal catecholamine 
secretion percentile between obese and lean animals. However, the percentile of 
catecholamine secretion stimulated by high K+ concentration was lower in the 
obese group. There was a decrease in the tyrosine hydroxylase enzyme expression 
(57.3%, P < 0.004) in adrenal glands of obese mice. Interestingly, the 
expression of dopamine beta-hydroxylase was also reduced (47.0%, P < 0.005). 
Phenylethanolamine N-methyltransferase expression was not affected. Our results 
show that in the MSG model, obesity status is associated with a defective 
adrenal chromaffin cell function. We conclude that in MSG obesity the low total 
catecholamine content is directly related to a decrease of key 
catecholamine-synthesizing enzymes, which by its turn may lead to a defective 
catecholamine secretion.