Linked Life Data

19619143

Source:http://linkedlifedata.com/resource/pubmed/id/19619143

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-9-11
pubmed:abstractText
Menopause is one of the triggers that induce obesity. Estradiol (E2), corticotropin-releasing hormone (CRH), and hypothalamic neuronal histamine are anorexigenic substances within the hypothalamus. This study examined the interactions among E2, CRH, and histamine during the regulation of feeding behavior and obesity in rodents. Food intake was measured in rats after the treatment of E2, alpha-fluoromethyl histidine, a specific suicide inhibitor of histidine decarboxylase that depletes hypothalamic neuronal histamine, or CRH antagonist. We measured food intake and body weight in wild-type mice or mice with targeted disruption of the histamine receptors (H1-R) knockout (H1KO mice). Furthermore, we investigated CRH content and histamine turnover in the hypothalamus after the E2 treatment or ovariectomy (OVX). We used immunohistochemical staining for estrogen receptors (ERs) in the histamine neurons. The E2-induced suppression of feeding was partially attenuated in rats pre-treated with alpha-fluoromethyl histidine or CRH antagonist and in H1KO mice. E2 treatment increased CRH content and histamine turnover in the hypothalamus. OVX increased food intake and body weight, and decreased CRH content and histamine turnover in the hypothalamus. In addition, E2 replacement reversed the OVX-induced changes in food intake and body weight in wild-type mice but not in H1KO mice. Immunohistochemical analysis revealed ERs were expressed on histamine neurons and western blotting analysis and pre-absorption study confirmed the specificity of ER antiserum we used. These results indicate that CRH and hypothalamic neuronal histamine mediate the suppressive effects of E2 on feeding behavior and body weight.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
110
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1796-805
pubmed:meshHeading
pubmed-meshheading:19619143-Analysis of Variance, pubmed-meshheading:19619143-Animals, pubmed-meshheading:19619143-Body Weight, pubmed-meshheading:19619143-Corticotropin-Releasing Hormone, pubmed-meshheading:19619143-Disease Models, Animal, pubmed-meshheading:19619143-Drug Interactions, pubmed-meshheading:19619143-Eating, pubmed-meshheading:19619143-Enzyme Inhibitors, pubmed-meshheading:19619143-Estradiol, pubmed-meshheading:19619143-Estrogens, pubmed-meshheading:19619143-Female, pubmed-meshheading:19619143-Histamine, pubmed-meshheading:19619143-Methylhistidines, pubmed-meshheading:19619143-Mice, pubmed-meshheading:19619143-Mice, Inbred C57BL, pubmed-meshheading:19619143-Mice, Knockout, pubmed-meshheading:19619143-Neurons, pubmed-meshheading:19619143-Obesity, pubmed-meshheading:19619143-Ovariectomy, pubmed-meshheading:19619143-Paraventricular Hypothalamic Nucleus, pubmed-meshheading:19619143-Rats, pubmed-meshheading:19619143-Rats, Sprague-Dawley, pubmed-meshheading:19619143-Receptors, Estrogen, pubmed-meshheading:19619143-Receptors, Histamine H1, pubmed-meshheading:19619143-Signal Transduction
pubmed:year
2009
pubmed:articleTitle
Hypothalamic neuronal histamine signaling in the estrogen deficiency-induced obesity.
pubmed:affiliation
Department of Internal Medicine 1, Faculty of Medicine, Oita University, Hasama, Yufu, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't