Document Detail


Autonomic and endocrine factors in the regulation of food intake.
MedLine Citation:
PMID:  2862966     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Destruction of the ventromedial hypothalamus produces hyperphagia, hyperinsulinemia and hypertriglyceridemia. These changes appear to be partly the result of increased firing rate of the vagus nerve and reduced firing rate of the sympathetic nerves. These reciprocal changes in the function of the autonomic nervous system appear to provide an adequate explanation for the hyperinsulinemia in this syndrome, and for the reduced heat expenditure. Destruction of the lateral hypothalamus, has effects opposite to those of the ventromedial hypothalamus with a reduction in food intake, a decrease in body fat, and an increase in the activity of the sympathetic nervous system. These reciprocal functions of the hypothalamus are associated with different adrenergic receptors. A medial hypothalamic alpha-adrenergic system mediates the epinephrine stimulation of feeding, and a beta-adrenergic system mediates the lateral hypothalamic inhibition of eating. Peptides from the endorphin family can stimulate food intake, but most other peptides are inhibitory. Growth hormone and thyroid hormone stimulate food intake under appropriate conditions. Insulin and adrenal steroids appear to play the most important role of all the hormones in regulating food intake. Deficiency of adrenal glucocorticoids is associated with decreased food intake and a wasting of body flesh. Increased levels of glucocorticoids, on the other hand, produce a variety of truncal obesity. In animals with ventromedial hypothalamic lesions and obesity, adrenalectomy will reverse the obesity. In genetically obese rats and mice, adrenalectomy will attenuate the progression of the syndrome. These effects appear to be through a reduction of food intake, and an increase in energy expenditure. Injections of insulin will stimulate food intake and may lead to obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
G A Bray
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Brain research bulletin     Volume:  14     ISSN:  0361-9230     ISO Abbreviation:  Brain Res. Bull.     Publication Date:  1985 Jun 
Date Detail:
Created Date:  1985-10-22     Completed Date:  1985-10-22     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  7605818     Medline TA:  Brain Res Bull     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  505-10     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adrenal Cortex Hormones / physiology
Animals
Autonomic Nervous System / physiology*
Eating* / drug effects
Gonadal Steroid Hormones / physiology
Growth Hormone / physiology
Hypothalamic Area, Lateral / physiology
Insulin / physiology
Neurosecretory Systems / physiology*
Neurotransmitter Agents / physiology
Sympathetic Nervous System / physiology
Thyroid Hormones / physiology
Ventromedial Hypothalamic Nucleus / physiology
Chemical
Reg. No./Substance:
0/Adrenal Cortex Hormones; 0/Gonadal Steroid Hormones; 0/Neurotransmitter Agents; 0/Thyroid Hormones; 11061-68-0/Insulin; 9002-72-6/Growth Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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