Document Detail


Apolipoprotein AIV requires cholecystokinin and vagal nerves to suppress food intake.
MedLine Citation:
PMID:  23027805     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apolipoprotein AIV (apo AIV) and cholecystokinin (CCK) are gastrointestinal satiation signals that are stimulated by fat consumption. Previous studies have demonstrated that peripheral apo AIV cannot cross the blood-brain barrier. In the present study, we hypothesized that peripheral apo AIV uses a CCK-dependent system and intact vagal nerves to relay its satiation signal to the hindbrain. To test this hypothesis, CCK-knockout (CCK-KO) mice and Long-Evan rats that had undergone subdiaphragmatic vagal deafferentation (SDA) were used. Intraperitoneal administration of apo AIV at 100 or 200 μg/kg suppressed food intake of wild-type (WT) mice at 30, 60, and 90 min. In contrast, the same dose did not reduce food intake in the CCK-KO mice. Blockade of the CCK 1 receptor by lorglumide, a CCK 1 receptor antagonist, attenuated apo AIV-induced satiation. Apo AIV at 100 μg/kg reduced food intake in SHAM rats but not in SDA rats. Furthermore, apo AIV elicited an increase in c-Fos-positive cells in the nucleus of the solitary tract (NTS), area postrema, dorsal motor nucleus of the vagus, and adjacent areas of WT mice but elicited only an attenuated increase in these same regions in CCK-KO mice. Apo AIV-induced c-Fos positive cells in the NTS and area postrema of WT mice were reduced by lorglumide. Lastly, apo AIV increased c-Fos positive cells in the NTS of SHAM rats but not in SDA rats. These observations imply that peripheral apo AIV requires an intact CCK system and vagal afferents to activate neurons in the hindbrain to reduce food intake.
Authors:
Chunmin C Lo; Wolfgang Langhans; Maria Georgievsky; Myrtha Arnold; Jody L Caldwell; Stacy Cheng; Min Liu; Stephen C Woods; Patrick Tso
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-01
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-29     Completed Date:  2013-01-31     Revised Date:  2013-12-04    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5857-65     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apolipoproteins A / metabolism*
Cholecystokinin / metabolism*
Eating
Feeding Behavior
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neurons / metabolism
Proto-Oncogene Proteins c-fos / metabolism
Rats
Rats, Long-Evans
Rhombencephalon / metabolism*
Time Factors
Vagus Nerve / metabolism*
Grant Support
ID/Acronym/Agency:
DK017844-35/DK/NIDDK NIH HHS; DK059630/DK/NIDDK NIH HHS; DK076928/DK/NIDDK NIH HHS; DK078201-04/DK/NIDDK NIH HHS; DK092138/DK/NIDDK NIH HHS; DK092779/DK/NIDDK NIH HHS; DK095440/DK/NIDDK NIH HHS; DK83550/DK/NIDDK NIH HHS; R01 DK092779/DK/NIDDK NIH HHS; R01 DK095440/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoproteins A; 0/Proto-Oncogene Proteins c-fos; 0/apolipoprotein A-IV; 9011-97-6/Cholecystokinin
Comments/Corrections

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