title: Crosstalk between angiogenesis, cytokeratin-18, and insulin resistance in the progression of non-alcoholic steatohepatitis.
abstract: OBJECTIVE
  To elucidate the possible crosstalk between angiogenesis, cytokeratin-18 (CK-18), and insulin resistance (IR) especially in patients with non-alcoholic steatohepatitis (NASH).
  
  
  METHODS
  Twenty-eight patients with NASH and 11 with simple fatty liver disease (FL) were enrolled in this study and underwent clinicopathological examination. The measures of angiogenesis, CK-18, and IR employed were CD34-immunopositive vessels, CK-18-immunopositive cells, and homeostasis model assessment of IR (HOMA-IR), respectively. The correlations of these factors with NASH were elucidated.
  
  
  RESULTS
  Significant development of hepatic neovascularization was observed only in NASH, whereas almost no neovascularization could be observed in FL and healthy liver. The degree of angiogenesis was almost parallel to liver fibrosis development, and both parameters were positively correlated. Similarly, CK-18 expression and HOMA-R were significantly increased in NASH as compared with FL and healthy liver. Furthermore, CK-18 and HOMA-IR were also positively correlated with the degree of neovascularization.
  
  
  CONCLUSIONS
  These results indicate that the crosstalk between angiogenesis, CK-18, and IR may play an important role in the onset and progression of NASH.
authors.affiliation: Third Department of Internal Medicine, Nara Medical University, Shijo-cho 840, Kashihara, Nara 634-8522, Japan.
authors.forename: Mitsuteru
authors.initials: M
authors.lastname: Kitade
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Yoshiji
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Noguchi
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Ikenaka
authors.forename: Kosuke
authors.initials: K
authors.lastname: Kaji
authors.forename: Yusaku
authors.initials: Y
authors.lastname: Shirai
authors.forename: Masaharu
authors.initials: M
authors.lastname: Yamazaki
authors.forename: Masahito
authors.initials: M
authors.lastname: Uemura
authors.forename: Junichi
authors.initials: J
authors.lastname: Yamao
authors.forename: Masao
authors.initials: M
authors.lastname: Fujimoto
authors.forename: Akira
authors.initials: A
authors.lastname: Mitoro
authors.forename: Masahisa
authors.initials: M
authors.lastname: Toyohara
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Sawai
authors.forename: Motoyuki
authors.initials: M
authors.lastname: Yoshida
authors.forename: Chie
authors.initials: C
authors.lastname: Morioka
authors.forename: Tatsuhiro
authors.initials: T
authors.lastname: Tsujimoto
authors.forename: Hideto
authors.initials: H
authors.lastname: Kawaratani
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Fukui
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D018450:Disease Progression; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D053538:Keratin-18 / Q000502:physiology*; D008099:Liver / Q000098:blood supply / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D053538:Keratin-18