On 2017 Nov 22, Sander Houten commented:

This paper focuses on the role of KLF14 in the regulation of hepatic gluconeogenesis in mice. The authors show that Klf14 mRNA and KLF14 protein expression in mouse liver is induced after overnight fasting. The authors furthermore show that Klf14 mRNA and KLF14 protein expression increased in liver of C57BL/6 mice on high fat diet, db/db mice and ob/ob mice when compared to control animals. The authors continue to demonstrate that the promoter of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (Pgc-1alpha), a transcriptional regulator of gluconeogenesis, contains one KLF14-binding site. In subsequent experiments the authors use adenovirus-mediated KLF14 overexpression and knockdown in isolated mouse hepatocytes and in vivo in mice, which further indicated that KLF14 modulates hepatic gluconeogenesis (Wang L, 2017).

I would like to point out that there is little evidence to support the hypothesis that KLF14 plays an important role in adult mouse liver biology. We found no evidence for expression of KLF14 in adult mouse liver as we were unable to amplify Klf14 cDNA, did not find Klf14 mapped reads in liver RNA sequencing data and found no specific signal upon immunoblotting (Argmann CA, 2017). Our data on the absence of Klf14 expression in liver are consistent with previously published work by others (Parker-Katiraee L, 2007) and publicly available data sources. We also investigated the physiological functions of KLF14 by studying a whole body KO mouse model and focused on the metabolic role of this transcription factor in mice on chow and high fat diet. Our results indicate that KLF14 does not play a role in the development of diet-induced insulin resistance in male C57BL/6 mice (Argmann CA, 2017).

On 2017 Nov 22, Sander Houten commented:

This paper focuses on the role of KLF14 in the regulation of hepatic gluconeogenesis in mice. The authors show that Klf14 mRNA and KLF14 protein expression in mouse liver is induced after overnight fasting. The authors furthermore show that Klf14 mRNA and KLF14 protein expression increased in liver of C57BL/6 mice on high fat diet, db/db mice and ob/ob mice when compared to control animals. The authors continue to demonstrate that the promoter of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (Pgc-1alpha), a transcriptional regulator of gluconeogenesis, contains one KLF14-binding site. In subsequent experiments the authors use adenovirus-mediated KLF14 overexpression and knockdown in isolated mouse hepatocytes and in vivo in mice, which further indicated that KLF14 modulates hepatic gluconeogenesis (Wang L, 2017).

I would like to point out that there is little evidence to support the hypothesis that KLF14 plays an important role in adult mouse liver biology. We found no evidence for expression of KLF14 in adult mouse liver as we were unable to amplify Klf14 cDNA, did not find Klf14 mapped reads in liver RNA sequencing data and found no specific signal upon immunoblotting (Argmann CA, 2017). Our data on the absence of Klf14 expression in liver are consistent with previously published work by others (Parker-Katiraee L, 2007) and publicly available data sources. We also investigated the physiological functions of KLF14 by studying a whole body KO mouse model and focused on the metabolic role of this transcription factor in mice on chow and high fat diet. Our results indicate that KLF14 does not play a role in the development of diet-induced insulin resistance in male C57BL/6 mice (Argmann CA, 2017).