Document Detail

Role of leptin in the control of feeding of goldfish Carassius auratus: interactions with cholecystokinin, neuropeptide Y and orexin A, and modulation by fasting.
MedLine Citation:
PMID:  12711082     Owner:  NLM     Status:  MEDLINE    
To assess the role of leptin on food intake regulation in goldfish, we examined the effects of central (intracerebroventricular, ICV) and peripheral (intraperitoneal, IP) injections of recombinant murine leptin on feeding behavior. Centrally (100 ng/g) and peripherally (300 ng/g) injected leptin both caused a significant decrease in food intake, compared to the saline-treated controls. To test the hypothesis that leptin influenced orexigenic neuropeptide systems in goldfish, fish were co-injected with neuropeptide Y (NPY) or orexin A and leptin. Both NPY (5 ng/g) and orexin A (10 ng/g) significantly increased food intake. Fish co-injected ICV with NPY (5 ng/g) or orexin A (10 ng/g) and leptin (1 or 10 ng/g) had a food intake lower than that of fish treated with NPY or orexin A alone. NPY mRNA expression in goldfish brain was reduced 2 and 6 h following central injection of leptin. To test the hypothesis that the cholecystokinin (CCK) mediates the effects of leptin in goldfish, fish were simultaneously injected ICV with an ineffective dose of leptin (10 ng/g) and either ICV or IP with an ineffective doses of CCK (1 ng/g ICV or 25 ng/g IP). These fish had a food intake lower than vehicle-treated fish, suggesting that leptin potentiates the satiety actions of CCK. CCK hypothalamic mRNA expression was increased 2 h following central treatment with leptin. The CCK receptor antagonist proglumide blocked both central and peripheral CCK satiety effects. Blockade of CCK brain receptors by proglumide resulted in an inhibition of the leptin-induced decrease in food intake and an attenuation of the inhibiting action of leptin on both NPY- and orexin A-induced feeding. These data suggests that CCK has a role in mediating the effects of leptin on food intake. Fasting potentiated the actions of leptin and attenuated the effects of CCK. Whereas fasting had no effects on the brain mRNA expression of CCK, it increased the brain mRNA expression of NPY and decreased the expression of CART. These changes in neuropeptide expression were partially reversed when fish were treated ICV with leptin. These results provide strong evidence that, in goldfish, leptin influences food intake, in part by modulating the orexigenic effects of NPY and orexin and that its actions are mediated, at least in part, by CCK.
Helene Volkoff; Angela Joy Eykelbosh; Richard Ector Peter
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Brain research     Volume:  972     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-04-24     Completed Date:  2003-07-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  90-109     Citation Subset:  IM    
Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada.
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MeSH Terms
Behavior, Animal
Carrier Proteins / metabolism*
Cholecystokinin / genetics,  metabolism*
DNA Probes / metabolism
Dose-Response Relationship, Drug
Drug Interactions
Eating / drug effects
Fasting / physiology*
Feeding Behavior / drug effects*,  physiology
Gene Expression Regulation / drug effects
Injections, Intraperitoneal / methods
Injections, Intraventricular / methods
Intracellular Signaling Peptides and Proteins*
Leptin / pharmacology*
Nerve Tissue Proteins / genetics
Neuropeptide Y / genetics,  metabolism*
Neuropeptides / metabolism*
Proglumide / pharmacology
RNA, Messenger / biosynthesis,  drug effects
Receptors, Cholecystokinin / antagonists & inhibitors
Receptors, G-Protein-Coupled
Receptors, Neuropeptide
Reverse Transcriptase Polymerase Chain Reaction / methods
Time Factors
Reg. No./Substance:
0/Carrier Proteins; 0/DNA Probes; 0/Intracellular Signaling Peptides and Proteins; 0/Leptin; 0/Nerve Tissue Proteins; 0/Neuropeptide Y; 0/Neuropeptides; 0/RNA, Messenger; 0/Receptors, Cholecystokinin; 0/Receptors, G-Protein-Coupled; 0/Receptors, Neuropeptide; 0/cocaine- and amphetamine-regulated transcript protein; 0/orexin receptors; 0/orexins; 6620-60-6/Proglumide; 9011-97-6/Cholecystokinin

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

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