Increased number of galanin-neurons in the paraventricular hypothalamic nucleus of neonatally overfed weanling rats

Perinatal overfeeding is a risk factor for overweight and diabetes during life. Underlying pathophysiological mechanisms are unclear. The peptide galanin is suggested to stimulate food intake by acting within the paraventricular hypothalamic nucleus (PVN). In early postnatally overfed rats overweigh...

Full description

Saved in:
Bibliographic Details
Published in:Brain research 1999-02, Vol.818 (1), p.160-163
Main Authors: Plagemann, Andreas, Harder, Thomas, Rake, Annett, Melchior, Kerstin, Rohde, Wolfgang, Dörner, Günter
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell Count
Feeding Behavior - physiology
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Galanin
Galanin - analysis
Hyperinsulinism - metabolism
Hyperinsulinism - pathology
Hypothalamus
Insulin
Neurons - chemistry
Neurons - cytology
Overweight
Paraventricular hypothalamic nucleus
Paraventricular Hypothalamic Nucleus - chemistry
Paraventricular Hypothalamic Nucleus - cytology
Perinatal overnutrition
Rats
Rats, Wistar
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Weaning
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Perinatal overfeeding is a risk factor for overweight and diabetes during life. Underlying pathophysiological mechanisms are unclear. The peptide galanin is suggested to stimulate food intake by acting within the paraventricular hypothalamic nucleus (PVN). In early postnatally overfed rats overweight and hyperinsulinemia were observed, accompanied by an increased number of galanin-positive neurons in the PVN at weaning. Our results might indicate malformation of hypothalamic galaninergic neurons due to neonatal overfeeding and hyperinsulinism, respectively, in rats.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(98)01264-5