title: Effect of immune stress on body weight regulation is altered by ovariectomy in female rats.
abstract: It has been suggested that obesity and loss of ovarian function alter the inflammatory response to immune stress. Ovariectomized (OVX) rats, which are used as a model of human menopause, exhibit both hyperphagia-induced obesity and gonadal steroid deficiency. To evaluate the effects of ovariectomy on inflammatory responses, we compared the anorectic response to LPS in OVX rats and gonad intact female rats. As leptin and hypothalamic interleukin-1β (IL1β) play pivotal roles in the anorectic response to immune stress, these factors were also measured. It was found that the OVX rats exhibited an increased anorectic response to LPS compared with the sham-operated rats. The OVX rats showed higher serum leptin concentrations and a greater increase in hypothalamic IL1β mRNA expression after LPS injection. In addition, in order to determine whether gonadal steroid deficiency contributes to the changes in the inflammatory responses of OVX rats, we compared responses between OVX rats treated with gonadal steroids and untreated OVX rats. There were no differences in appetite, the serum leptin level, and hypothalamic IL1β mRNA expression between the two groups after LPS injection. These findings suggest that the loss of ovarian function increases the induction of leptin and hypothalamic IL1β synthesis and consequently increases the anorectic response under immune stress conditions. It is possible that these alterations are caused by OVX-induced obesity rather than the direct effects of gonadal steroid deficiency.
authors.affiliation: Department of Obstetrics and Gynecology, The University of Tokushima Graduate School, Institute of Health Biosciences, 3-18-15 Kuramoto-Cho, Tokushima 770-8503, Japan. iwasa1976@gmail.com
authors.forename: Takeshi
authors.initials: T
authors.lastname: Iwasa
authors.forename: Toshiya
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: Riyo
authors.initials: R
authors.lastname: Kinouchi
authors.forename: Ganbat
authors.initials: G
authors.lastname: Gereltsetseg
authors.forename: Masahiro
authors.initials: M
authors.lastname: Murakami
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakazawa
authors.forename: Shinobu
authors.initials: S
authors.lastname: Fujisawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Akira
authors.initials: A
authors.lastname: Kuwahara
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Yasui
authors.forename: Minoru
authors.initials: M
authors.lastname: Irahara
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006801:Humans; D007031:Hypothalamus / Q000276:immunology / Q000378:metabolism; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000276:immunology; D020738:Leptin / Q000097:blood / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008593:Menopause / Q000097:blood / Q000276:immunology; D008954:Models, Biological; D010052:Ovariectomy; D010053:Ovary / Q000276:immunology* / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological / Q000276:immunology*
chemical_list: D053583:Interleukin-1beta; D020738:Leptin; D008070:Lipopolysaccharides; D012333:RNA, Messenger