The afferent signals that evoke changes in energy intake with regard to body weight regulation are presumed to arise partly from body stores, with the most likely candidate being adipose tissue depots. However, clinical investigation of the neuronal circuitry involved in the central nervous system's processing of such satiety signals remains largely unexplored. Using percutaneously placed catheters in either the right or left internal jugular veins, we were able to quantify the release of central nervous system monoamine and indoleamine neurotransmitters in 64 weight-stable male subjects with varying degrees of adiposity. Veno-arterial plasma concentration differences and internal jugular blood or plasma flow were used, according to the Fick Principle, to quantify the amount of neurotransmitter stemming from the brain. By combining this technique with a noradrenaline and adrenaline isotope dilution method for examining neuronal transmitter release, we were able to examine the association between central nervous system neurotransmitters and efferent sympathetic nervous outflow and adrenomedullary function in human obesity. We found that brain 5-hydroxytryptamine (serotonin) turnover is chronically elevated in proportion to adiposity and is increased postprandially to a similar degree in lean and obese individuals. There was no difference in the degree of sympathetic nervous activity or rate of adrenaline secretion in the subjects examined. It therefore seems that in human obesity, in the face of a chronic elevation in peripheral satiety signals, brain serotonergic processes are switched on accordingly, but the subsequent physiological response involving a reduction in food intake, increased thermogenesis and sympathetic activity is in some way impeded.
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February 1999
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Research Article|
February 01 1999
Human obesity is associated with a chronic elevation in brain 5-hydroxytryptamine turnover
Gavin W. LAMBERT;
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
Correspondence: Dr G. Lambert.
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Mario VAZ;
Mario VAZ
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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Helen S. COX;
Helen S. COX
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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Andrea G. TURNER;
Andrea G. TURNER
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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David M. KAYE;
David M. KAYE
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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Garry L. JENNINGS;
Garry L. JENNINGS
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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Murray D. ESLER
Murray D. ESLER
1Human Autonomic Function Laboratory, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia
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Publisher: Portland Press Ltd
Received:
May 28 1998
Revision Received:
September 14 1998
Accepted:
September 30 1998
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 1999
1999
Clin Sci (Lond) (1999) 96 (2): 191–197.
Article history
Received:
May 28 1998
Revision Received:
September 14 1998
Accepted:
September 30 1998
Citation
Gavin W. LAMBERT, Mario VAZ, Helen S. COX, Andrea G. TURNER, David M. KAYE, Garry L. JENNINGS, Murray D. ESLER; Human obesity is associated with a chronic elevation in brain 5-hydroxytryptamine turnover. Clin Sci (Lond) 1 February 1999; 96 (2): 191–197. doi: https://doi.org/10.1042/cs0960191
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