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Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression
BACKGROUND: Abnormal hepatic gluconeogenesis is related to hyperglycemia in mammals with insulin resistance. Despite the strong evidences linking Krüppel-like factor 11 (KLF11) gene mutations to development of Type 2 diabetes, the precise physiological functions of KLF11 in vivo remain largely unkno...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935883/ https://www.ncbi.nlm.nih.gov/pubmed/24586865 http://dx.doi.org/10.1371/journal.pone.0089552 |
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author | Zhang, Huabing Chen, Qi Jiao, Tao Cui, Anfang Sun, Xiujing Fang, Weijun Xie, Liwei Liu, Yang Fang, Fude Chang, Yongsheng |
author_facet | Zhang, Huabing Chen, Qi Jiao, Tao Cui, Anfang Sun, Xiujing Fang, Weijun Xie, Liwei Liu, Yang Fang, Fude Chang, Yongsheng |
author_sort | Zhang, Huabing |
collection | PubMed |
description | BACKGROUND: Abnormal hepatic gluconeogenesis is related to hyperglycemia in mammals with insulin resistance. Despite the strong evidences linking Krüppel-like factor 11 (KLF11) gene mutations to development of Type 2 diabetes, the precise physiological functions of KLF11 in vivo remain largely unknown. RESULTS: In current investigation, we showed that KLF11 is involved in modulating hepatic glucose metabolism in mice. Overexpression of KLF11 in primary mouse hepatocytes could inhibit the expression of gluconeogenic genes, including phosphoenolpyruvate carboxykinase (cytosolic isoform, PEPCK-C) and peroxisome proliferator–activated receptor γ coactivator-1α (PGC-1α), subsequently decreasing the cellular glucose output. Diabetic mice with overexpression of KLF11 gene in livers significantly ameliorated hyperglycemia and glucose intolerance; in contrast, the knockdown of KLF11 expression in db/m and C57BL/6J mice livers impaired glucose tolerance. CONCLUSIONS: Our data strongly indicated the involvement of KLF11 in hepatic glucose homeostasis via modulating the expression of PEPCK-C. |
format | Online Article Text |
id | pubmed-3935883 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-39358832014-03-04 Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression Zhang, Huabing Chen, Qi Jiao, Tao Cui, Anfang Sun, Xiujing Fang, Weijun Xie, Liwei Liu, Yang Fang, Fude Chang, Yongsheng PLoS One Research Article BACKGROUND: Abnormal hepatic gluconeogenesis is related to hyperglycemia in mammals with insulin resistance. Despite the strong evidences linking Krüppel-like factor 11 (KLF11) gene mutations to development of Type 2 diabetes, the precise physiological functions of KLF11 in vivo remain largely unknown. RESULTS: In current investigation, we showed that KLF11 is involved in modulating hepatic glucose metabolism in mice. Overexpression of KLF11 in primary mouse hepatocytes could inhibit the expression of gluconeogenic genes, including phosphoenolpyruvate carboxykinase (cytosolic isoform, PEPCK-C) and peroxisome proliferator–activated receptor γ coactivator-1α (PGC-1α), subsequently decreasing the cellular glucose output. Diabetic mice with overexpression of KLF11 gene in livers significantly ameliorated hyperglycemia and glucose intolerance; in contrast, the knockdown of KLF11 expression in db/m and C57BL/6J mice livers impaired glucose tolerance. CONCLUSIONS: Our data strongly indicated the involvement of KLF11 in hepatic glucose homeostasis via modulating the expression of PEPCK-C. Public Library of Science 2014-02-26 /pmc/articles/PMC3935883/ /pubmed/24586865 http://dx.doi.org/10.1371/journal.pone.0089552 Text en © 2014 Zhang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Zhang, Huabing Chen, Qi Jiao, Tao Cui, Anfang Sun, Xiujing Fang, Weijun Xie, Liwei Liu, Yang Fang, Fude Chang, Yongsheng Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title | Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title_full | Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title_fullStr | Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title_full_unstemmed | Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title_short | Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression |
title_sort | involvement of klf11 in hepatic glucose metabolism in mice via suppressing of pepck-c expression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935883/ https://www.ncbi.nlm.nih.gov/pubmed/24586865 http://dx.doi.org/10.1371/journal.pone.0089552 |
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