Reviewer's report
Title:The FLS (Fatty liver Shionogi) mouse reveals local expressions of
lipocalin-2, CXCL1 and CXCL9 in the liver with non-alcoholic steatohepatitis
Version: 2Date:3 May 2013
Reviewer: Manlio Vinciguerra
Reviewer's report:
The study from Semba et al. aims at identifying differential markers of NASH, not
espressed in steatosis, using the Fatty liver Shionogi mouse model. Microarray
analysis is used to identify 3 molecules, adipokines/chemokines that correlate
well with inflammatory properties as determined by WB and IHC. The authors
propose that these 3 markers, and in particolar LCN2, could play significant roles
in the progression from steatosis to NASH. The study is linear, well designed and
the data are of good quality.
I have though several comments:
It would be better to introduce, starting from the abstract, the concept of non
alcoholic fatty liver diseases (NAFLD), which includes the spectrum ranging from
simple steatosis, to NASH, to HCC. Within NAFLD this study aims to elucidate
the differences between steatosis and NASH etc etc
Methods (abstract): Immunohistochemistry can not be used to detect gene
expression, rephrase
Results (abstract): DNA microarray analyses can not reveal proteins, rephrase
DS and FLS, apart the citations of references, are not adequately described.
What is the mutation inducing NASH phenotype? What makes the “sister” strain
DS developing steatosis but not NASH? How they originate from each other?
A more detailed analysis of microarray analysis, cut off criteria should be
described in the text, not in supplemental, as well as Table III, so that scientists
can try to analyse the GEO data with the same criteria.
Discussion: the two-hit hypothesis is now considered obsolete, considering the
role of the gut microbiota and the new mechanisms discovered (Podrini C, Curr
Pharm Des 2013). The authors should re-formulate this paragraph. Adipokines
and citokines should be discussed in the modern frame of knowledge.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests
Reviewer's report
Title:The FLS (Fatty liver Shionogi) mouse reveals local expressions of
lipocalin-2, CXCL1 and CXCL9 in the liver with non-alcoholic steatohepatitis
Version: 2Date:3 May 2013
Reviewer: Manlio Vinciguerra
Reviewer's report:
The study from Semba et al. aims at identifying differential markers of NASH, not
espressed in steatosis, using the Fatty liver Shionogi mouse model. Microarray
analysis is used to identify 3 molecules, adipokines/chemokines that correlate
well with inflammatory properties as determined by WB and IHC. The authors
propose that these 3 markers, and in particolar LCN2, could play significant roles
in the progression from steatosis to NASH. The study is linear, well designed and
the data are of good quality.
I have though several comments:
It would be better to introduce, starting from the abstract, the concept of non
alcoholic fatty liver diseases (NAFLD), which includes the spectrum ranging from
simple steatosis, to NASH, to HCC. Within NAFLD this study aims to elucidate
the differences between steatosis and NASH etc etc
Methods (abstract): Immunohistochemistry can not be used to detect gene
expression, rephrase
Results (abstract): DNA microarray analyses can not reveal proteins, rephrase
DS and FLS, apart the citations of references, are not adequately described.
What is the mutation inducing NASH phenotype? What makes the “sister” strain
DS developing steatosis but not NASH? How they originate from each other?
A more detailed analysis of microarray analysis, cut off criteria should be
described in the text, not in supplemental, as well as Table III, so that scientists
can try to analyse the GEO data with the same criteria.
Discussion: the two-hit hypothesis is now considered obsolete, considering the
role of the gut microbiota and the new mechanisms discovered (Podrini C, Curr
Pharm Des 2013). The authors should re-formulate this paragraph. Adipokines
and citokines should be discussed in the modern frame of knowledge.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests
Please review this paper.
user
Reviewer's report
Title:The FLS (Fatty liver Shionogi) mouse reveals local expressions of
lipocalin-2, CXCL1 and CXCL9 in the liver with non-alcoholic steatohepatitis
Version: 2Date:3 May 2013
Reviewer: Manlio Vinciguerra
Reviewer's report:
The study from Semba et al. aims at identifying differential markers of NASH, not
espressed in steatosis, using the Fatty liver Shionogi mouse model. Microarray
analysis is used to identify 3 molecules, adipokines/chemokines that correlate
well with inflammatory properties as determined by WB and IHC. The authors
propose that these 3 markers, and in particolar LCN2, could play significant roles
in the progression from steatosis to NASH. The study is linear, well designed and
the data are of good quality.
I have though several comments:
It would be better to introduce, starting from the abstract, the concept of non
alcoholic fatty liver diseases (NAFLD), which includes the spectrum ranging from
simple steatosis, to NASH, to HCC. Within NAFLD this study aims to elucidate
the differences between steatosis and NASH etc etc
Methods (abstract): Immunohistochemistry can not be used to detect gene
expression, rephrase
Results (abstract): DNA microarray analyses can not reveal proteins, rephrase
DS and FLS, apart the citations of references, are not adequately described.
What is the mutation inducing NASH phenotype? What makes the “sister” strain
DS developing steatosis but not NASH? How they originate from each other?
A more detailed analysis of microarray analysis, cut off criteria should be
described in the text, not in supplemental, as well as Table III, so that scientists
can try to analyse the GEO data with the same criteria.
Discussion: the two-hit hypothesis is now considered obsolete, considering the
role of the gut microbiota and the new mechanisms discovered (Podrini C, Curr
Pharm Des 2013). The authors should re-formulate this paragraph. Adipokines
and citokines should be discussed in the modern frame of knowledge.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests
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