Reviewer's report
Title:Effect of intracellular lipid accumulation in a new model of non-alcoholic
fatty liver disease
Version: 1Date:3 December 2011
Reviewer: Marco Arrese
Reviewer's report:
Chavez-Tapia et al. report on their results using an in vitro model of non-alcoholic
fatty liver (NAFLD) which consist in exposing a cell line to increasing
concentrations of palmitic and oleic acid. This maneuver determines an increase
the intracellular content of lipid droplets and results in increased gene expression
of interleukin-6, interleukin-8 and tumor necrosis factor alpha as well as of genes
related to hepatic fibrogenesis. Also, the authors found that in their model
exposure to free fatty acids is associated to oxidative stress and apoptosis. The
paper is overall of good quality and provides information using a somewhat novel
approach. It is well written and the methodology is appropriate. My comments are
as it follows.
MAJOR COMMENTS
As the authors mentioned in the discussion section, this study contains
proof-of-concept data supporting a role of fatty acids in evoking both
inflammatory and fibrogenic responses in an in vitro model of NAFLD. Although
not entirely novel the findings are well substantiated and the scientific merit is
enough to consider this paper acceptable for publication.
MINOR COMMENTS:
1. Abbreviations for Non-alcoholic fatty liver disease and non-alcoholic
steatohepatitis are not introduced in the abstract.
2. Abbreviation non-alcoholic steatohepatitis should be introduced in the last
paragraph of the introduction.
3. There is some confusion with figure labeling and supplemental files.
Figure 1 is fine.
Figure 2 is fine
Figure 3 is referred in the text (Figure legends page 18) as “Fibrogenic cytokines
mRNA expression” but actually correspond to inflammatory cytokines protein
production.
Figure 4 is referred in the text (Figure legends page 18) as “Apoptosis induction
secondary to fatty acids toxicity” but actually correspond to Fibrogenic cytokines
mRNA expression.
Supplementary Figure 1 is not inflammatory cytokines protein production but
increased reactive oxygen species in cells treated with fatty acids.
Supplementary Figure 2.is not increased reactive oxygen species in cells treated
with fatty acids.
4. The authors may want to include some recent references related to their work:
a) A recent and closely related work which shows complementary data to the
present study: Cellular glutathione in fatty liver in vitro models Toxicology in Vitro
25 (2011) 1501–1506
b) Recent reviews on Lipotoxicity should also be included and commented (i.e.
Trauner M, Arrese M, Wagner M Fatty liver and lipotoxicity. Biochim Biophys
Acta. 2010;1801:299-310 and Ibrahim SH, Kohli R, Gores GJ. Mechanisms of
Lipotoxicity in NAFLD and clinical implications.J Pediatr Gastroenterol Nutr.
2011;53:131-40
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I know thecorresponding author and have one joint publication with him this year;
this is however someonelse's paper (neither myself nor the referred author are
the corresponding authors nor work together). We also do not have current
established collaborations. Thus, I feel that that I have no competing interests
with regard to the present work.
Reviewer's report
Title:Effect of intracellular lipid accumulation in a new model of non-alcoholic
fatty liver disease
Version: 1Date:3 December 2011
Reviewer: Marco Arrese
Reviewer's report:
Chavez-Tapia et al. report on their results using an in vitro model of non-alcoholic
fatty liver (NAFLD) which consist in exposing a cell line to increasing
concentrations of palmitic and oleic acid. This maneuver determines an increase
the intracellular content of lipid droplets and results in increased gene expression
of interleukin-6, interleukin-8 and tumor necrosis factor alpha as well as of genes
related to hepatic fibrogenesis. Also, the authors found that in their model
exposure to free fatty acids is associated to oxidative stress and apoptosis. The
paper is overall of good quality and provides information using a somewhat novel
approach. It is well written and the methodology is appropriate. My comments are
as it follows.
MAJOR COMMENTS
As the authors mentioned in the discussion section, this study contains
proof-of-concept data supporting a role of fatty acids in evoking both
inflammatory and fibrogenic responses in an in vitro model of NAFLD. Although
not entirely novel the findings are well substantiated and the scientific merit is
enough to consider this paper acceptable for publication.
MINOR COMMENTS:
1. Abbreviations for Non-alcoholic fatty liver disease and non-alcoholic
steatohepatitis are not introduced in the abstract.
2. Abbreviation non-alcoholic steatohepatitis should be introduced in the last
paragraph of the introduction.
3. There is some confusion with figure labeling and supplemental files.
Figure 1 is fine.
Figure 2 is fine
Figure 3 is referred in the text (Figure legends page 18) as “Fibrogenic cytokines
mRNA expression” but actually correspond to inflammatory cytokines protein
production.
Figure 4 is referred in the text (Figure legends page 18) as “Apoptosis induction
secondary to fatty acids toxicity” but actually correspond to Fibrogenic cytokines
mRNA expression.
Supplementary Figure 1 is not inflammatory cytokines protein production but
increased reactive oxygen species in cells treated with fatty acids.
Supplementary Figure 2.is not increased reactive oxygen species in cells treated
with fatty acids.
4. The authors may want to include some recent references related to their work:
a) A recent and closely related work which shows complementary data to the
present study: Cellular glutathione in fatty liver in vitro models Toxicology in Vitro
25 (2011) 1501–1506
b) Recent reviews on Lipotoxicity should also be included and commented (i.e.
Trauner M, Arrese M, Wagner M Fatty liver and lipotoxicity. Biochim Biophys
Acta. 2010;1801:299-310 and Ibrahim SH, Kohli R, Gores GJ. Mechanisms of
Lipotoxicity in NAFLD and clinical implications.J Pediatr Gastroenterol Nutr.
2011;53:131-40
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I know thecorresponding author and have one joint publication with him this year;
this is however someonelse's paper (neither myself nor the referred author are
the corresponding authors nor work together). We also do not have current
established collaborations. Thus, I feel that that I have no competing interests
with regard to the present work.
Please review this paper.
user
Reviewer's report
Title:Effect of intracellular lipid accumulation in a new model of non-alcoholic
fatty liver disease
Version: 1Date:3 December 2011
Reviewer: Marco Arrese
Reviewer's report:
Chavez-Tapia et al. report on their results using an in vitro model of non-alcoholic
fatty liver (NAFLD) which consist in exposing a cell line to increasing
concentrations of palmitic and oleic acid. This maneuver determines an increase
the intracellular content of lipid droplets and results in increased gene expression
of interleukin-6, interleukin-8 and tumor necrosis factor alpha as well as of genes
related to hepatic fibrogenesis. Also, the authors found that in their model
exposure to free fatty acids is associated to oxidative stress and apoptosis. The
paper is overall of good quality and provides information using a somewhat novel
approach. It is well written and the methodology is appropriate. My comments are
as it follows.
MAJOR COMMENTS
As the authors mentioned in the discussion section, this study contains
proof-of-concept data supporting a role of fatty acids in evoking both
inflammatory and fibrogenic responses in an in vitro model of NAFLD. Although
not entirely novel the findings are well substantiated and the scientific merit is
enough to consider this paper acceptable for publication.
MINOR COMMENTS:
1. Abbreviations for Non-alcoholic fatty liver disease and non-alcoholic
steatohepatitis are not introduced in the abstract.
2. Abbreviation non-alcoholic steatohepatitis should be introduced in the last
paragraph of the introduction.
3. There is some confusion with figure labeling and supplemental files.
Figure 1 is fine.
Figure 2 is fine
Figure 3 is referred in the text (Figure legends page 18) as “Fibrogenic cytokines
mRNA expression” but actually correspond to inflammatory cytokines protein
production.
Figure 4 is referred in the text (Figure legends page 18) as “Apoptosis induction
secondary to fatty acids toxicity” but actually correspond to Fibrogenic cytokines
mRNA expression.
Supplementary Figure 1 is not inflammatory cytokines protein production but
increased reactive oxygen species in cells treated with fatty acids.
Supplementary Figure 2.is not increased reactive oxygen species in cells treated
with fatty acids.
4. The authors may want to include some recent references related to their work:
a) A recent and closely related work which shows complementary data to the
present study: Cellular glutathione in fatty liver in vitro models Toxicology in Vitro
25 (2011) 1501–1506
b) Recent reviews on Lipotoxicity should also be included and commented (i.e.
Trauner M, Arrese M, Wagner M Fatty liver and lipotoxicity. Biochim Biophys
Acta. 2010;1801:299-310 and Ibrahim SH, Kohli R, Gores GJ. Mechanisms of
Lipotoxicity in NAFLD and clinical implications.J Pediatr Gastroenterol Nutr.
2011;53:131-40
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I know thecorresponding author and have one joint publication with him this year;
this is however someonelse's paper (neither myself nor the referred author are
the corresponding authors nor work together). We also do not have current
established collaborations. Thus, I feel that that I have no competing interests
with regard to the present work.
assistant