Reviewer's report
Title:Hepatitis C virus E2 protein involve in insulin resistance through an
impairment of Akt/PKB and GSK3beta signaling in hepatocytes
Version: 2Date:9 May 2012
Reviewer: yuan-soon ho
Reviewer's report:
The manuscript from Hsieh et al. describes the potential role of E2 protein from
HCV genotype 1b in T2DM. The authors have investigated the effects of HCV E2
on insulin signaling, and found that E2 has the ability to induce insulin resistance.
The manuscript provided some interesting aspects of E2 function, especially with
respect to SOCS3 upregulation. However, there are several defects in the data
and their interpretation. My comments on the manuscript were as mentioned
below.
Major criticisms:
1. Ikuo Shoji published a very nice paper in 2011 (Shoji et al, 2011) showing that
HCV-induced down-regulation of GLUT2 expression and up-regulation of
gluconeogenesis. This suggests that high concentration of glucose in
HCV-infected hepatocytes, although interpretation of their data should be
cautioned because they used a HCV J6/JFH1-infected cells. It seems that this
too could be part of the discussion in this manuscript.
2. Figure 2 does not show much significant difference in IRS-1 status. Moreover,
the actin bands too strong to make it difficult for loading comparison. The
immunoblots should be done more clear, and quantification of each bands need
to be done more precisely, with SD.
3. Figure 4: The effect of MG132 was not very significant. The immunoblots
should be done more clear, it would help to include scanned data with lower actin
level for proper comparison.
4. In Figure 5, the mark of phosphorylation is confusing. Please use uniform style
for phosphorylation of Akt and GSK3beta in all figures and quantification of each
band.
Minor criticisms:
In Figure 2C and 6B, the statistical analysis should be done between FLAG and
E2.
Level of interest: An article of outstanding merit and interest in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
Reviewer's report
Title:Hepatitis C virus E2 protein involve in insulin resistance through an
impairment of Akt/PKB and GSK3beta signaling in hepatocytes
Version: 2Date:9 May 2012
Reviewer: yuan-soon ho
Reviewer's report:
The manuscript from Hsieh et al. describes the potential role of E2 protein from
HCV genotype 1b in T2DM. The authors have investigated the effects of HCV E2
on insulin signaling, and found that E2 has the ability to induce insulin resistance.
The manuscript provided some interesting aspects of E2 function, especially with
respect to SOCS3 upregulation. However, there are several defects in the data
and their interpretation. My comments on the manuscript were as mentioned
below.
Major criticisms:
1. Ikuo Shoji published a very nice paper in 2011 (Shoji et al, 2011) showing that
HCV-induced down-regulation of GLUT2 expression and up-regulation of
gluconeogenesis. This suggests that high concentration of glucose in
HCV-infected hepatocytes, although interpretation of their data should be
cautioned because they used a HCV J6/JFH1-infected cells. It seems that this
too could be part of the discussion in this manuscript.
2. Figure 2 does not show much significant difference in IRS-1 status. Moreover,
the actin bands too strong to make it difficult for loading comparison. The
immunoblots should be done more clear, and quantification of each bands need
to be done more precisely, with SD.
3. Figure 4: The effect of MG132 was not very significant. The immunoblots
should be done more clear, it would help to include scanned data with lower actin
level for proper comparison.
4. In Figure 5, the mark of phosphorylation is confusing. Please use uniform style
for phosphorylation of Akt and GSK3beta in all figures and quantification of each
band.
Minor criticisms:
In Figure 2C and 6B, the statistical analysis should be done between FLAG and
E2.
Level of interest: An article of outstanding merit and interest in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
Please review this paper.
user
Reviewer's report
Title:Hepatitis C virus E2 protein involve in insulin resistance through an
impairment of Akt/PKB and GSK3beta signaling in hepatocytes
Version: 2Date:9 May 2012
Reviewer: yuan-soon ho
Reviewer's report:
The manuscript from Hsieh et al. describes the potential role of E2 protein from
HCV genotype 1b in T2DM. The authors have investigated the effects of HCV E2
on insulin signaling, and found that E2 has the ability to induce insulin resistance.
The manuscript provided some interesting aspects of E2 function, especially with
respect to SOCS3 upregulation. However, there are several defects in the data
and their interpretation. My comments on the manuscript were as mentioned
below.
Major criticisms:
1. Ikuo Shoji published a very nice paper in 2011 (Shoji et al, 2011) showing that
HCV-induced down-regulation of GLUT2 expression and up-regulation of
gluconeogenesis. This suggests that high concentration of glucose in
HCV-infected hepatocytes, although interpretation of their data should be
cautioned because they used a HCV J6/JFH1-infected cells. It seems that this
too could be part of the discussion in this manuscript.
2. Figure 2 does not show much significant difference in IRS-1 status. Moreover,
the actin bands too strong to make it difficult for loading comparison. The
immunoblots should be done more clear, and quantification of each bands need
to be done more precisely, with SD.
3. Figure 4: The effect of MG132 was not very significant. The immunoblots
should be done more clear, it would help to include scanned data with lower actin
level for proper comparison.
4. In Figure 5, the mark of phosphorylation is confusing. Please use uniform style
for phosphorylation of Akt and GSK3beta in all figures and quantification of each
band.
Minor criticisms:
In Figure 2C and 6B, the statistical analysis should be done between FLAG and
E2.
Level of interest: An article of outstanding merit and interest in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
assistant