Document Detail


Nesfatin-1(30-59) but not the N- and C-terminal fragments, nesfatin-1(1-29) and nesfatin-1(60-82) injected intracerebroventricularly decreases dark phase food intake by increasing inter-meal intervals in mice.
MedLine Citation:
PMID:  22682899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nesfatin-1 is an 82 amino acid N-terminal fragment of nucleobindin2 that was consistently shown to reduce dark phase food intake upon brain injection in rodents. We recently reported that nesfatin-1(1-82) injected intracerebroventricularly (icv) reduces dark phase feeding in mice. Moreover, intraperitoneal injection of mid-fragment nesfatin-1 (nesfatin-1(30-59)) mimics the food intake-reducing effects of nesfatin-1(1-82), whereas N-terminal (nesfatin-1(1-29)) and C-terminal fragments (nesfatin-1(60-82)) did not. We therefore characterized the structure-activity relationship of nesfatin-1 injected icv to influence the dark phase meal pattern in mice. Mouse nesfatin-1(1-29), nesfatin-1(30-59), nesfatin-1(60-82) or vehicle was injected icv in freely fed C57Bl/6 mice immediately before the dark phase and food intake was monitored using an automated episodic feeding monitoring system. Nesfatin-1(30-59) (0.1, 0.3, 0.9 nmol/mouse) induced a dose-related reduction of 4-h food intake by 28%, 49% and 49% respectively resulting in a 23% decreased cumulative 24-h food intake compared to vehicle at the 0.3 nmol/mouse dose (p<0.05). The peak reduction occurred during the 3rd (-96%) and 4th hour (-91%) post injection and was associated with a reduced meal frequency (0-4h: -47%) and prolonged inter-meal intervals (3.1-times) compared to vehicle (p<0.05), whereas meal size was not altered. In contrast, neither nesfatin-1(1-29) nor nesfatin-1(60-82) reduced dark phase food intake at equimolar doses although nesfatin-1(60-82) prolonged inter-meal intervals (1.7-times, p<0.05). Nesfatin-1(30-59) is the active core of nesfatin-1(1-82) to induce satiety indicated by a reduced meal number during the first 4h post injection. The delayed onset may be indicative of time required to modulate other hypothalamic and medullary networks regulating nocturnal feeding as established for nesfatin-1.
Authors:
Andreas Stengel; Miriam Goebel-Stengel; Lixin Wang; Ikuo Kato; Masatomo Mori; Yvette Taché
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-03-28
Journal Detail:
Title:  Peptides     Volume:  35     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-11     Completed Date:  2012-11-19     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  United States    
Other Details:
Languages:  eng     Pagination:  143-8     Citation Subset:  IM    
Copyright Information:
Published by Elsevier Inc.
Affiliation:
CURE/Digestive Diseases Research Center, Center for Neurobiology of Stress, Digestive Diseases Division, Department of Medicine, University of California Los Angeles, Los Angeles, CA 90073, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / drug effects,  physiology
Calcium-Binding Proteins / administration & dosage,  chemistry,  pharmacology*
DNA-Binding Proteins / administration & dosage,  chemistry,  pharmacology*
Eating / drug effects,  physiology
Feeding Behavior / drug effects*
Injections, Intraventricular
Male
Mice
Mice, Inbred C57BL
Nerve Tissue Proteins / administration & dosage,  chemistry,  pharmacology*
Peptide Fragments / administration & dosage,  pharmacology
Photoperiod
Structure-Activity Relationship
Grant Support
ID/Acronym/Agency:
DK-41301/DK/NIDDK NIH HHS; P30 DK041301-13/DK/NIDDK NIH HHS; R01 DK-33061/DK/NIDDK NIH HHS; R01 DK033061-27/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/DNA-Binding Proteins; 0/Nerve Tissue Proteins; 0/Peptide Fragments; 0/nucleobindin
Comments/Corrections

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


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