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KLF9 Regulates PGC1α Expression and Its Function in Gluconeogenesis

Author: NiuDong
Tutor: FangFuDe；ChangYongSheng
School: Beijing Union Medical College
Course: Biochemistry and Molecular Biology
Keywords: PGC1α KLF9 Gluconeogenesis PPARγ CIDEC Transcriptional regulation
CLC: R346
Type: Master's thesis
Year: 2011
Downloads: 44
Quote: 0
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Abstract


The first portion KLF9 on PGC1a Expression regulation and role in gluconeogenesis in hepatic glucose XENOBIOTIC very necessary to the survival of the organism prolonged hunger case, but in the case of diabetes is non-normal open. Known transcriptional co-activator factor peroxisome proliferator receptor Y coactivator 1 (PGC1a) play an important physiological function in this process. PGC1a is an the gluconeogenesis gene upstream regulatory factors activate the expression of these enzymes play an important regulatory function. PGC1a cAMP pathway and activation of the transcription factor CREB regulation. KLF9 Kruppel-like factors zinc finger protein family, also known as the basal transcription sequence binding protein 1 (BTEB1), is a combination of high GC sequence of the transcription factor structure. KLF9 can regulate the expression of the progesterone receptor (PR), its absence will reduce the sensitivity of the uterus PR target genes for progesterone, leading to low fertility. The liver, KLF9 combination promote Hnf4a adjusting the role of thyroid hormones in the liver. KLF9 PPARγ promoter, capable of binding to the regulation of adipose tissue development. By in vivo and in vitro experiments, we proved the expression of PGC1a KLF9 capable of binding to PGC1a promoter and regulation, in turn, regulate the expression levels of the liver enzymes of gluconeogenesis. Reduce KLF9 expression in diabetic mice, can effectively improve the body's sensitivity to insulin, and the cause of diabetes, high blood sugar has improved effect. In this study, the first to demonstrate the the KLF9 function in the body's glucose metabolism. The second part PGC1a with PPARy total to activate cidec the express CIDEC of genes is another important member of the the CIDE family involved in the body's fat metabolism synthesis. Reports about it focuses on role of CIDEC fat generation process. Whose expression levels were significantly increased during adipocyte differentiation. Recent studies indicate CIDEC gene can to promote cell triglyceride generate and stimulate lipid droplets increase. PPARγ is a member of the PPAR (Peroxisome Proliferator-Activated Receptor) family. It can form a heterodimer with RXR, through the combination of the PPRE elements on the DNA promoter gene expression regulation. PPARy is a key transcription factor responsible for regulating fat synthesis in the liver, lower expression in the liver, and cause the occurrence of fatty liver once overexpression. In this study, by constructing 5 'deletion cut the original mutation and cis-promoter, using dual fluorescent reporter gene assay PPARy HepG2 cells and (?) (?) GC1a the CIDEC common activation and to determine the original cis-acting. PPARy the specific agonists pioglitazone stimulus 3T3-L1 cells detected (?) CIDEC (?) Level. The the nRNA check CIDEC, measured fat synthesis and energy metabolism gene overexpression level in 3T3-L1 cell line. MRNA cell in mouse liver primary fine fat changes in expression in the detection of liver cells by adenovirus infection. The ultimate proof the CIDEC, and PPARy can significantly PGCla activated promoter, caused by the accumulation of fat in the body. CIDEC

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