title: Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity.
abstract: 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.
authors.affiliation: Department of Cell Biology and Genetics, State University of Maringá, Maringá, PR, Brazil.
authors.forename: Andréia C P
authors.initials: AC
authors.lastname: Martins
authors.forename: Kléber L A
authors.initials: KL
authors.lastname: Souza
authors.forename: Marina T
authors.initials: MT
authors.lastname: Shio
authors.forename: Paulo C F
authors.initials: PC
authors.lastname: Mathias
authors.forename: Peter I
authors.initials: PI
authors.lastname: Lelkes
authors.forename: Raúl M G
authors.initials: RM
authors.lastname: Garcia
mesh_terms: D000313:Adrenal Medulla / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D004195:Disease Models, Animal; D004299:Dopamine beta-Hydroxylase / Q000096:biosynthesis; D005260:Female; D007027:Hypothalamic Diseases / Q000139:chemically induced / Q000150:complications*; D051379:Mice; D006899:Mixed Function Oxygenases / Q000096:biosynthesis*; D009765:Obesity / Q000201:enzymology / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D010625:Phenylethanolamine N-Methyltransferase / Q000096:biosynthesis*; D012970:Sodium Glutamate / Q000633:toxicity; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis
chemical_list: D002395:Catecholamines; D006899:Mixed Function Oxygenases; D014446:Tyrosine 3-Monooxygenase; D004299:Dopamine beta-Hydroxylase; D010625:Phenylethanolamine N-Methyltransferase; D012970:Sodium Glutamate