title: Hormonal synchronization of lipopolysaccharide-induced hypothermic response in rats.
abstract: BACKGROUND
  Recent experimental evidence suggests that lipopolysaccharide (LPS)-induced hypothermia is an adaptive thermoregulatory strategy against immunological challenge in rats. We hypothesized that the hormones which are predominantly responsible for energy homeostasis may have efferent signaling roles for development of the hypothermia.
  
  
  OBJECTIVE
  The aim of the study was to evaluate the changes of hypothalamic-pituitary-thyroid (HPT) and hypothalamic- pituitary-adrenal (HPA) axis hormones, leptin and erythropoietin at various phases of LPS-induced hypothermia such as the initial phase, nadir and the end of the response in blood sampled rats.
  
  
  METHODS
  Body temperature of adult male albino Wistar rats was recorded by biotelemetry. E. coli O111:B4 LPS (250 μg/kg, ip) was injected alone or with SC-560, a cyclooxygenase-1 selective inhibitor (1 mg/kg, sc).
  
  
  RESULTS
  Serum FT4 levels elevated at the initial phase, but FT3 levels decreased at nadir and remained low at the end of the response. Meanwhile, no change was observed in TSH levels. Serum adrenocorticotropic hormone (ACTH) levels reduced at the initial phase and serum corticosterone levels decreased at nadir without any change in serum corticotropin-releasing hormone (CRH) levels throughout the hypothermia. Serum leptin levels increased only at the end of the response. No change was observed in the levels of serum erythropoietin. SC-560 treatment abolished both LPS-induced hypothermia and respective hormonal changes.
  
  
  CONCLUSIONS
  Data suggest that HPT axis hormones may contribute to development of LPS-induced hypothermia in rats. Data also support the view that leptin may have a role for the recovery of hypothermic response.
authors.affiliation: Aksaray University, Faculty of Art and Science, Department of Biology, 68100 Aksaray, Turkey. polat.hsyn@hotmail.com.
authors.forename: H
authors.initials: H
authors.lastname: Polat
authors.forename: S
authors.initials: S
authors.lastname: Mamuk
authors.forename: E S
authors.initials: ES
authors.lastname: Akarsu
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000032:analysis*; D001831:Body Temperature / Q000187:drug effects*; D003345:Corticosterone / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004921:Erythropoietin / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000378:metabolism; D007035:Hypothermia / Q000139:chemically induced / Q000378:metabolism*; D020738:Leptin / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051379:Mice; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000378:metabolism; D011720:Pyrazoles / Q000494:pharmacology; D017208:Rats, Wistar; D013972:Thyrotropin / Q000378:metabolism; D013974:Thyroxine / Q000378:metabolism
chemical_list: D015415:Biomarkers; D016861:Cyclooxygenase Inhibitors; D020738:Leptin; D008070:Lipopolysaccharides; D011720:Pyrazoles; C115461:SC 560; D004921:Erythropoietin; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D013974:Thyroxine; D003345:Corticosterone