Hepatic senescence marker protein-30 is involved in the progression of nonalcoholic fatty liver disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-11-28

AUTHORS

Hyohun Park, Akihito Ishigami, Toshihide Shima, Masayuki Mizuno, Naoki Maruyama, Kanji Yamaguchi, Hironori Mitsuyoshi, Masahito Minami, Kohichiroh Yasui, Yoshito Itoh, Toshikazu Yoshikawa, Michiaki Fukui, Goji Hasegawa, Naoto Nakamura, Mitsuhiro Ohta, Hiroshi Obayashi, Takeshi Okanoue

ABSTRACT

BackgroundBoth insulin resistance and increased oxidative stress in the liver are associated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Senescence marker protein-30 (SMP30) was initially identified as a novel protein in the rat liver, and acts as an antioxidant and antiapoptotic protein. Our aim was to determine whether hepatic SMP30 levels are associated with the development and progression of NAFLD.MethodsLiver biopsies and blood samples were obtained from patients with an NAFLD activity score (NAS) ≤ 2 (n = 18), NAS of 3–4 (n = 14), and NAS ≥ 5 (n = 66).ResultsPatients with NAS ≥ 5 had significantly lower hepatic SMP30 levels (12.5 ± 8.4 ng/mg protein) than patients with NAS ≤ 2 (30.5 ± 14.2 ng/mg protein) and patients with NAS = 3–4 (24.6 ± 12.2 ng/mg protein). Hepatic SMP30 decreased in a fibrosis stage-dependent manner. Hepatic SMP30 levels were correlated positively with the platelet count (r = 0.291) and negatively with the homeostasis model assessment of insulin resistance (r = −0.298), the net electronegative charge modified-low-density lipoprotein (r = −0.442), and type IV collagen 7S (r = −0.350). The immunostaining intensity levels of 4-hydroxynonenal in the liver were significantly and inversely correlated with hepatic SMP30 levels. Both serum large very low-density lipoprotein (VLDL) and very small low-density lipoprotein (LDL) levels in patients with NAS ≥ 5 were significantly higher than those seen in patients with NAS ≤ 2, and these lipoprotein fractions were significantly and inversely correlated with hepatic SMP30.ConclusionThese results suggest that hepatic SMP30 is closely associated with the pathogenesis of NAFLD, although it is not known whether decreased hepatic SMP30 is a result or a cause of cirrhosis. More... »

PAGES

426-434

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00535-009-0154-3

DOI

http://dx.doi.org/10.1007/s00535-009-0154-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039812213

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19946731


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27 schema:description BackgroundBoth insulin resistance and increased oxidative stress in the liver are associated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Senescence marker protein-30 (SMP30) was initially identified as a novel protein in the rat liver, and acts as an antioxidant and antiapoptotic protein. Our aim was to determine whether hepatic SMP30 levels are associated with the development and progression of NAFLD.MethodsLiver biopsies and blood samples were obtained from patients with an NAFLD activity score (NAS) ≤ 2 (n = 18), NAS of 3–4 (n = 14), and NAS ≥ 5 (n = 66).ResultsPatients with NAS ≥ 5 had significantly lower hepatic SMP30 levels (12.5 ± 8.4 ng/mg protein) than patients with NAS ≤ 2 (30.5 ± 14.2 ng/mg protein) and patients with NAS = 3–4 (24.6 ± 12.2 ng/mg protein). Hepatic SMP30 decreased in a fibrosis stage-dependent manner. Hepatic SMP30 levels were correlated positively with the platelet count (r = 0.291) and negatively with the homeostasis model assessment of insulin resistance (r = −0.298), the net electronegative charge modified-low-density lipoprotein (r = −0.442), and type IV collagen 7S (r = −0.350). The immunostaining intensity levels of 4-hydroxynonenal in the liver were significantly and inversely correlated with hepatic SMP30 levels. Both serum large very low-density lipoprotein (VLDL) and very small low-density lipoprotein (LDL) levels in patients with NAS ≥ 5 were significantly higher than those seen in patients with NAS ≤ 2, and these lipoprotein fractions were significantly and inversely correlated with hepatic SMP30.ConclusionThese results suggest that hepatic SMP30 is closely associated with the pathogenesis of NAFLD, although it is not known whether decreased hepatic SMP30 is a result or a cause of cirrhosis.
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