Catecholamine Metabolism in Primary Anorexia Nervosa
The Journal of Clinical Endocrinology & MetabolismPublished 1 December 1979
Howard A. Gross, C. Raymond Lake, Michael H. Ebert, Michael G. Ziegler, Irwin J. Kopin
Citations147
SJR quartileQ1
SJR score2.18
SNIP1.77
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TL;DR
The results suggest that abnormalities in catecholamine metabolism in primary anorexia nervosa are caused by starvation, and that neuronal functions dependent on aminergic neurotransmission may be altered as a result.
Abstract
Abnormalities in neuroendocrine function and sympathetic nervous system activity appear to be present in primary anorexia nervosa. Hypothalamic catecholamines are involved in control of endocrine function and norepinephrine is released from sympathetic nerve endings. Because of possible abnormalities in catecholamine metabolism, plasma levels of norepinephrine and urinary excretion of homovanillic acid and 3-methoxy-4-hydroxyphenyl glycol were studied in female patients with primary anorexia nervosa before and after significant clinical improvement and compared with normal female volunteers. During the phase of the disease in which body weights were more than 20--25% below ideal, patients' blood pressures and pulse rates, plasma levels of norepinephrine, and 24-h urinary excretion of 3-methoxy-4-hydroxyphenol glycol and homovanillic acid were lower than those of a group of normal volunteers. After weight gain, these parameters increased to near-normal levels. At no time was plasma dopamine-beta-hydroxylase activity abnormal. The results suggest that abnormalities in catecholamine metabolism in primary anorexia nervosa are caused by starvation, and that neuronal functions dependent on aminergic neurotransmission may be altered as a result.
Keywords
Psychology
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