title: Neonatal LPS injection alters the body weight regulation systems of rats under non-stress and immune stress conditions.
abstract: It has been reported that prenatal immune stress induced by lipopolysaccharides or cytokines increases food intake and leads to obesity and other features of metabolic syndrome in adulthood. Using Sprague-Dawley rats, we evaluated whether neonatal LPS injection altered their body weight regulation systems under non-stress and immune stress conditions. On Day 10 after birth, all pups were injected with LPS (100 microg/kg, i.p.) (PND(10)LPS) or saline (PND(10)Saline). After weaning, body weight was significantly elevated in PND(10)LPS compared with PND(10)Saline. Thereafter, the rats were injected with LPS (100 microg/kg, i.p.) or saline (used as a basal condition) from 7 to 8 weeks of age. Under basal conditions, cumulative food intake were significantly higher, serum leptin concentration was significantly increased, and hypothalamic NPY mRNA expression was significantly decreased in PND(10)LPS compared with PND(10)Saline. Under adult LPS injected conditions, body weight gain and cumulative food intake were suppressed in both the PND(10)LPS and PND(10)Saline groups compared with those observed under basal adult saline-injected conditions. The suppressive effects induced by adult LPS injection were less evident in the PND(10)LPS group than in the PND(10)Saline group. Adult LPS injection increased the serum leptin concentration in the PND(10)Saline rats, but not in the PND(10)LPS rats. In addition, adult LPS injection increased the mRNA expression of anorexinergic factors (IL-1beta, and TNF-alpha), and decreased that of the orexinergic factor NPY in both groups. However, the influence of adult LPS injection upon these factors was less evident in the PND(10)LPS group than in the PND(10)Saline group. These results suggest that neonatal LPS injection alters body weight regulation under both non-stress and immune stress conditions in male rats. Changes in the endocrine, neuropeptide, and cytokine regulation systems might be involved in these alterations.
authors.affiliation: Department of Obstetrics and Gynecology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan. takeshi1@clin.med.tokushima-u.ac.jp
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: Shinobu
authors.initials: S
authors.lastname: Fujisawa
authors.forename: Masahiro
authors.initials: M
authors.lastname: Murakami
authors.forename: Machiko
authors.initials: M
authors.lastname: Kiyokawa
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: D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight / Q000276:immunology* / Q000502:physiology*; D003345:Corticosterone / Q000097:blood; D005247:Feeding Behavior / Q000502:physiology; D007031:Hypothalamus / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D009478:Neuropeptide Y / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D020738:Leptin; D008070:Lipopolysaccharides; D009478:Neuropeptide Y; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D003345:Corticosterone