Dehydroepiandrosterone (DHEA) blocks the increase in food intake caused by neuropeptide Y (NPY) in the Zucker rat

Recent studies have demonstrated that neuropeptide Y (NPY) reduced the neural production of dehydroepiandrosterone (DHEA) in frog hypothalamic explants. The objective of this study was to assess if DHEA can block the NPY induced increase in food intake in lean and obese Zucker rats. Rats were given...

Full description

Saved in:
Bibliographic Details
Published inNutritional neuroscience Vol. 9; no. 5-6; pp. 225 - 232
Main Authors Navar, Daniel, S'Aulis, Dana, Corll, Connie, Svec, Frank, Porter, Johnny R.
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 01.10.2006
Subjects
Animal Feed
Animals
Anura
DEHYDROEPIANDROSTERONE
Dehydroepiandrosterone - pharmacology
Dose-Response Relationship, Drug
Energy Intake - drug effects
Female
FOOD INTAKE
NEUROPEPTIDE Y
Neuropeptide Y - physiology
Obesity - genetics
Obesity - physiopathology
Rats
Rats, Zucker
SEROTONIN
VENTROMEDIAL HYPOTHALAMUS
Online AccessGet full text

Cover

More Information
Summary:Recent studies have demonstrated that neuropeptide Y (NPY) reduced the neural production of dehydroepiandrosterone (DHEA) in frog hypothalamic explants. The objective of this study was to assess if DHEA can block the NPY induced increase in food intake in lean and obese Zucker rats. Rats were given one of the following four treatments: sterile water/dimethylsulfoxide (DMSO), NPY/DMSO, water/DHEA, and NPY/DHEA. Immediately after administration of their respective treatment, rats were exposed to macronutrients for 4 h and food intake was monitored. NPY caused a significant increase in total calories consumed compared to control. Co-administration of DHEA along with NPY blocked this NPY dependent effect. These results suggest that DHEA blocks the over-eating in satiated rats induced by NPY. Measurement of changes in regional hypothalamic and raphe monoamine neurotransmitters known to affect food intake suggested a possible role of serotonin fluctuations in the ventromedial hypothalamus (VMH) guiding this behaviour.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1028-415X
1476-8305
DOI:10.1080/10284150601090102