title: Vulnerability of experimentally induced fatty liver to heat stress in rats.
abstract: BACKGROUND
  The aim of this study was to confirm the vulnerability of fatty liver to heat stress using fatty liver rats from the viewpoint of the induction of apoptosis.
  
  
  METHODS
  We exposed rats with and without a fatty liver to heat stress and then looked for apoptotic cells within the liver tissue using two apoptosis detection kits. We also determined the mRNA expression of heat shock protein (HSP) 70, caspase-3, bcl-2, and bax using a quantitative reverse transcription-polymerase chain reaction method.
  
  
  RESULTS
  Following heat stress, apoptosis was strongly visible in the fatty liver comparing with that noted in the normal liver. The expression of HSP70 was increased following heat stress in both livers, but the volume of its expression was significantly less in the fatty liver than in the normal liver. The ratio of bcl-2/bax expression tended to increase in the normal liver but decrease in the fatty liver following heat stress. Caspase-3 demonstrated no significant change following heat stress in both livers.
  
  
  CONCLUSIONS
  The detection of apoptosis, together with changes in the mRNA expression of HSP70 and the expression ratio bcl-2/bax mRNA may indicate vulnerability of a fatty liver to heat stress and may support the hypothesis that morphologic change is induced in a fatty liver by exposure to heat stress. These results suggest that fatty liver may be more vulnerable to heat stress than normal liver.
authors.affiliation: Department of Forensic Pathology and Sciences, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Inoue
authors.forename: Naomi
authors.initials: N
authors.lastname: Sameshima
authors.forename: Tomomi
authors.initials: T
authors.lastname: Ishida
authors.forename: Akiko
authors.initials: A
authors.lastname: Tsuji
authors.forename: Keiko
authors.initials: K
authors.lastname: Kudo
authors.forename: Noriaki
authors.initials: N
authors.lastname: Ikeda
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D004792:Enzyme Precursors; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D015870:Gene Expression; D018882:Heat Stress Disorders / Q000150:complications*; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D004792:Enzyme Precursors; D006360:Heat-Shock Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases