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Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice. / Argmann, Carmen A.; Violante, Sara; Dodatko, Tetyana et al.

In: BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, Vol. 1863, No. 12, 2017, p. 3277-3285.

Research output: Contribution to journal › Article › Academic › peer-review

Harvard

Argmann, CA, Violante, S, Dodatko, T, Amaro, MP, Hagen, J, Gillespie, VL, Buettner, C, Schadt, EE & Houten, SM 2017, 'Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice', BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, vol. 1863, no. 12, pp. 3277-3285. https://doi.org/10.1016/j.bbadis.2017.09.021

APA

Argmann, C. A., Violante, S., Dodatko, T., Amaro, M. P., Hagen, J., Gillespie, V. L., Buettner, C., Schadt, E. E., & Houten, S. M. (2017). Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice. BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 1863(12), 3277-3285. https://doi.org/10.1016/j.bbadis.2017.09.021

Vancouver

Argmann CA, Violante S, Dodatko T, Amaro MP, Hagen J, Gillespie VL et al. Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice. BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS. 2017;1863(12):3277-3285. Epub 2017. doi: 10.1016/j.bbadis.2017.09.021

Author

Argmann, Carmen A. ; Violante, Sara ; Dodatko, Tetyana et al. / Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice. In: BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS. 2017 ; Vol. 1863, No. 12. pp. 3277-3285.

BibTeX

@article{495401e8bcb94b4f8d152597f16057df,
title = "Germline deletion of Kr{\"u}ppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice",
abstract = "The transcription factor Kr{\"u}ppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model. Male whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels. KLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14(+/+) and Klf14(-/-) mice on chow and HFD. We found that in mice expression of Klf14 was the highest in the anterior pituitary (adenohypophysis), lower but detectable in white adipose tissue and undetectable in liver. Loss of KLF14 function impacted on the pituitary transcriptome with extracellular matrix organization as the primary affected pathway and a predicted link to glucocorticoid receptor signaling. Whole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans",
author = "Argmann, {Carmen A.} and Sara Violante and Tetyana Dodatko and Amaro, {Mariana P.} and Jacob Hagen and Gillespie, {Virginia L.} and Christoph Buettner and Schadt, {Eric E.} and Houten, {Sander M.}",
year = "2017",
doi = "10.1016/j.bbadis.2017.09.021",
language = "English",
volume = "1863",
pages = "3277--3285",
journal = "BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS",
issn = "0005-2728",
publisher = "Elsevier",
number = "12",

}

RIS

TY - JOUR

T1 - Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice

AU - Argmann, Carmen A.

AU - Violante, Sara

AU - Dodatko, Tetyana

AU - Amaro, Mariana P.

AU - Hagen, Jacob

AU - Gillespie, Virginia L.

AU - Buettner, Christoph

AU - Schadt, Eric E.

AU - Houten, Sander M.

PY - 2017

Y1 - 2017

N2 - The transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model. Male whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels. KLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14(+/+) and Klf14(-/-) mice on chow and HFD. We found that in mice expression of Klf14 was the highest in the anterior pituitary (adenohypophysis), lower but detectable in white adipose tissue and undetectable in liver. Loss of KLF14 function impacted on the pituitary transcriptome with extracellular matrix organization as the primary affected pathway and a predicted link to glucocorticoid receptor signaling. Whole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans

AB - The transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model. Male whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels. KLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14(+/+) and Klf14(-/-) mice on chow and HFD. We found that in mice expression of Klf14 was the highest in the anterior pituitary (adenohypophysis), lower but detectable in white adipose tissue and undetectable in liver. Loss of KLF14 function impacted on the pituitary transcriptome with extracellular matrix organization as the primary affected pathway and a predicted link to glucocorticoid receptor signaling. Whole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans

U2 - 10.1016/j.bbadis.2017.09.021

DO - 10.1016/j.bbadis.2017.09.021

M3 - Article

C2 - 28962896

VL - 1863

SP - 3277

EP - 3285

JO - BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS

JF - BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS

SN - 0005-2728

IS - 12

ER -

ID: 4101238