单位：[1]Anhui Med Univ, Sch Basic Med, Dept Biochem & Mol Biol, Hefei, Peoples R China[2]Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100730, Peoples R China[3]Peking Union Med Coll, Beijing 100021, Peoples R China[4]Jining Med Univ, Dept Biochem, Jining, Peoples R China[5]Capital Med Univ, Beijing Friendship Hosp, Beijing Digest Dis Ctr, Beijing Key Lab Precancerous Les Digest Dis, Beijing, Peoples R China临床科室国家中心消化分中心首都医科大学附属北京友谊医院[6]Anhui Med Univ, Sch Basic Med, Dept Chem, Hefei, Peoples R China[7]Univ Michigan, Ann Arbor, MI 48109 USA[8]Liaoning Univ Tradit Chinese Med, Hosp Affiliated, Dept Endocrinol, Shenyang, Peoples R China
Background: Abnormal hepatic gluconeogenesis is related to hyperglycemia in mammals with insulin resistance. Despite the strong evidences linking Kruppel-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 c coactivator-1 alpha (PGC-1 alpha), 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.
基金：
Peking Union Medical College (PUMC); Fundamental Research Funds for the Central UniversitiesFundamental Research Funds for the Central Universities [3332013108]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31371193, 30872992]; Scientific Research of BSKY [XJ201301]; Anhui Medical University [2013xkj004]
第一作者单位：[1]Anhui Med Univ, Sch Basic Med, Dept Biochem & Mol Biol, Hefei, Peoples R China[2]Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100730, Peoples R China[3]Peking Union Med Coll, Beijing 100021, Peoples R China
通讯作者：
推荐引用方式(GB/T 7714)：
Zhang Huabing,Chen Qi,Jiao Tao,et al.Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression[J].PLOS ONE.2014,9(2):doi:10.1371/journal.pone.0089552.
APA：
Zhang, Huabing,Chen, Qi,Jiao, Tao,Cui, Anfang,Sun, Xiujing...&Chang, Yongsheng.(2014).Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression.PLOS ONE,9,(2)
MLA：
Zhang, Huabing,et al."Involvement of KLF11 in Hepatic Glucose Metabolism in Mice via Suppressing of PEPCK-C Expression".PLOS ONE 9..2(2014)
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