Apoptosis in rat jejunal mucosa is regulated partly through the central nervous system, which controls feeding behavior

Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small intestines. Methods:  The test solutions used in this study were an H1 receptor antagonist (chlorpheniramine maleate), 2‐deoxy‐D‐glucose, leptin, and 1‐deox...

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Published inJournal of gastroenterology and hepatology Vol. 20; no. 8; pp. 1285 - 1291
Main Authors LIN, TAISAN, SAKATA, HIROYUKI, OOTANI, AKIFUMI, FUJISE, TAKEHIRO, TSUNADA, SEIJI, AMEMORI, SADAHIRO, DANJO, AKIKO, YOKOYAMA, FUMIE, SAKATA, YASUHISA, IWAKIRI, RYUICHI, TODA, SHUJI, FUJIMOTO, KAZUMA
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LanguageEnglish
Published Melbourne, Australia Blackwell Science Pty 01.08.2005
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Abstract Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small intestines. Methods:  The test solutions used in this study were an H1 receptor antagonist (chlorpheniramine maleate), 2‐deoxy‐D‐glucose, leptin, and 1‐deoxy‐D‐glucosamine (2‐amino‐1,5‐anhydro‐2‐deoxy‐D‐glucitol). Test solutions were injected into the third cerebroventricles of rats. Feeding behavior and jejunal apoptosis were evaluated both with and without truncal vagotomy. Intestinal apoptosis was evaluated by percentage fragmented DNA, electrophoresis, and TUNEL staining. Results:  Chlorpheniramine and 2‐deoxy‐D‐glucose elicited feeding, whereas leptin and 1‐deoxy‐D‐glucosamine suppressed feeding. The test solutions, which elicited feeding (0.24 and 24 µmol/rat of chlorpheniramine and 2‐deoxy‐D‐glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In contrast, the test solutions, which suppressed feeding (8 and 24 µmol/rat of leptin and 1‐deoxy‐D‐glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy. Conclusion:  The central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis.
AbstractList Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small intestines. Methods:  The test solutions used in this study were an H1 receptor antagonist (chlorpheniramine maleate), 2‐deoxy‐D‐glucose, leptin, and 1‐deoxy‐D‐glucosamine (2‐amino‐1,5‐anhydro‐2‐deoxy‐D‐glucitol). Test solutions were injected into the third cerebroventricles of rats. Feeding behavior and jejunal apoptosis were evaluated both with and without truncal vagotomy. Intestinal apoptosis was evaluated by percentage fragmented DNA, electrophoresis, and TUNEL staining. Results:  Chlorpheniramine and 2‐deoxy‐D‐glucose elicited feeding, whereas leptin and 1‐deoxy‐D‐glucosamine suppressed feeding. The test solutions, which elicited feeding (0.24 and 24 µmol/rat of chlorpheniramine and 2‐deoxy‐D‐glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In contrast, the test solutions, which suppressed feeding (8 and 24 µmol/rat of leptin and 1‐deoxy‐D‐glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy. Conclusion:  The central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis.
Abstract Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small intestines. Methods:  The test solutions used in this study were an H 1 receptor antagonist (chlorpheniramine maleate), 2‐deoxy‐D‐glucose, leptin, and 1‐deoxy‐D‐glucosamine (2‐amino‐1,5‐anhydro‐2‐deoxy‐D‐glucitol). Test solutions were injected into the third cerebroventricles of rats. Feeding behavior and jejunal apoptosis were evaluated both with and without truncal vagotomy. Intestinal apoptosis was evaluated by percentage fragmented DNA, electrophoresis, and TUNEL staining. Results:  Chlorpheniramine and 2‐deoxy‐D‐glucose elicited feeding, whereas leptin and 1‐deoxy‐D‐glucosamine suppressed feeding. The test solutions, which elicited feeding (0.24 and 24 µmol/rat of chlorpheniramine and 2‐deoxy‐D‐glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In contrast, the test solutions, which suppressed feeding (8 and 24 µmol/rat of leptin and 1‐deoxy‐D‐glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy. Conclusion:  The central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis.
The aim of this study was to investigate whether central nervous system-related feeding behavior regulates mucosal apoptosis in rat small intestines. The test solutions used in this study were an H(1) receptor antagonist (chlorpheniramine maleate), 2-deoxy-D-glucose, leptin, and 1-deoxy-D-glucosamine (2-amino-1,5-anhydro-2-deoxy-D-glucitol). Test solutions were injected into the third cerebroventricles of rats. Feeding behavior and jejunal apoptosis were evaluated both with and without truncal vagotomy. Intestinal apoptosis was evaluated by percentage fragmented DNA, electrophoresis, and TUNEL staining. Chlorpheniramine and 2-deoxy-D-glucose elicited feeding, whereas leptin and 1-deoxy-D-glucosamine suppressed feeding. The test solutions, which elicited feeding (0.24 and 24 micromol/rat of chlorpheniramine and 2-deoxy-D-glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In contrast, the test solutions, which suppressed feeding (8 and 24 micromol/rat of leptin and 1-deoxy-D-glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy. The central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis.
AIMThe aim of this study was to investigate whether central nervous system-related feeding behavior regulates mucosal apoptosis in rat small intestines.METHODSThe test solutions used in this study were an H(1) receptor antagonist (chlorpheniramine maleate), 2-deoxy-D-glucose, leptin, and 1-deoxy-D-glucosamine (2-amino-1,5-anhydro-2-deoxy-D-glucitol). Test solutions were injected into the third cerebroventricles of rats. Feeding behavior and jejunal apoptosis were evaluated both with and without truncal vagotomy. Intestinal apoptosis was evaluated by percentage fragmented DNA, electrophoresis, and TUNEL staining.RESULTSChlorpheniramine and 2-deoxy-D-glucose elicited feeding, whereas leptin and 1-deoxy-D-glucosamine suppressed feeding. The test solutions, which elicited feeding (0.24 and 24 micromol/rat of chlorpheniramine and 2-deoxy-D-glucose, respectively), suppressed mucosal apoptosis in the rat jejunum 1 h after cerebroventricular infusion. In contrast, the test solutions, which suppressed feeding (8 and 24 micromol/rat of leptin and 1-deoxy-D-glucosamine, respectively), induced jejunal mucosal apoptosis 3 h after infusion. The effects of the test solutions on feeding behavior and changes in apoptosis were not affected by truncal vagotomy.CONCLUSIONThe central nervous system, which regulates feeding behavior, might control intestinal function through the regulation of intestinal apoptosis.
Author OOTANI, AKIFUMI
FUJIMOTO, KAZUMA
LIN, TAISAN
DANJO, AKIKO
IWAKIRI, RYUICHI
AMEMORI, SADAHIRO
TSUNADA, SEIJI
SAKATA, YASUHISA
YOKOYAMA, FUMIE
FUJISE, TAKEHIRO
SAKATA, HIROYUKI
TODA, SHUJI
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Issue 8
Keywords Brain
Trunk
Glucosamine
Rat
Mucosa
percentage fragmented DNA
Central nervous system
Check
Hypothalamus
brain gut axis
Antihistaminic
Small intestine
Encephalon
Prevention
Regulation(control)
Jejunum
Electrophoresis
Antagonist
Antirheumatic agent
Chlorphenamine
Feeding behavior
vagal nerve
Rodentia
Gut
feeding center
Feeding
Vertebrata
Mammalia
Animal
DNA
H1 Histamine receptor
Apoptosis
Language English
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Snippet Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small intestines....
The aim of this study was to investigate whether central nervous system-related feeding behavior regulates mucosal apoptosis in rat small intestines. The test...
Abstract Aim:  The aim of this study was to investigate whether central nervous system‐related feeding behavior regulates mucosal apoptosis in rat small...
AIMThe aim of this study was to investigate whether central nervous system-related feeding behavior regulates mucosal apoptosis in rat small...
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StartPage 1285
SubjectTerms Animals
Apoptosis - physiology
Biological and medical sciences
Bones, joints and connective tissue. Antiinflammatory agents
Brain Chemistry
brain gut axis
Central Nervous System - drug effects
Central Nervous System - physiology
Chlorpheniramine - administration & dosage
Chlorpheniramine - pharmacology
Deoxyglucose - administration & dosage
Deoxyglucose - pharmacology
Feeding Behavior - drug effects
Feeding Behavior - physiology
feeding center
Histamine H1 Antagonists - administration & dosage
Histamine H1 Antagonists - pharmacology
hypothalamus
Hypothalamus - physiology
Intestinal Mucosa - cytology
Intestinal Mucosa - drug effects
Intestinal Mucosa - innervation
Jejunum - drug effects
Jejunum - innervation
Jejunum - metabolism
Leptin - pharmacology
Male
Medical sciences
percentage fragmented DNA
Pharmacology. Drug treatments
Rats
Rats, Sprague-Dawley
vagal nerve
Vagotomy
Title Apoptosis in rat jejunal mucosa is regulated partly through the central nervous system, which controls feeding behavior
URI https://api.istex.fr/ark:/67375/WNG-XJN7LJ6S-G/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1440-1746.2005.03921.x
https://www.ncbi.nlm.nih.gov/pubmed/16048579
https://search.proquest.com/docview/68082574
Volume 20
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