Abstract:
:Recently fibroblast growth factor 21 (FGF21) has been identified as a potent regulator in glucose and lipid homeostasis. Here, we firstly investigated the metabolic role of FGF21 in human liver-derived HepG2 cells, and suggested that overexpression of FGF21 suppressed triglyceride accumulation by inhibiting the transcription of the gene necessary for de novo lipogenesis. The potential mechanism of FGF21 regulating lipogenesis was also explored, which revealed that FGF21 repressed the transcription of sterol regulatory element binding protein 1c (SREBP1c), an essential transcription factor promoting expression of lipogenesis-related genes. Overexpression of FGF21 ameliorated the up-regulation of SREBP1c and fatty acid synthase (FAS) in HepG2 cells elicited by FFAs treatment. Moreover, FGF21 could inhibit the transcriptional levels of the key genes involved in processing and nuclear translocation of SREBP1c, and decrease the protein amount of mature SREBP1c. Unexpectedly, overexpression of SREBP1c in HepG2 cells could also inhibit the endogenous FGF21 transcription. Further experiments demonstrated that SREBP1c could significantly attenuate the promoter activity of FGF21. In conclusion, our data identifies a clear link between FGF21 and SREBP1c during lipogenesis in hepatocyte in culture.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Zhang Y,Lei T,Huang JF,Wang SB,Zhou LL,Yang ZQ,Chen XDdoi
10.1016/j.mce.2011.05.003subject
Has Abstractpub_date
2011-08-06 00:00:00pages
41-7issue
1-2eissn
0303-7207issn
1872-8057pii
S0303-7207(11)00244-9journal_volume
342pub_type
杂志文章abstract::The effects of prostaglandins (PGs) on rat pineal metabolism were examined in vitro. PGE2 (0.01-1 microM) increased the activity of serotonin-N-acetyltransferase (SNAT), the stimulation curve exhibiting a maximum at 0.1 microM. PGE1 increased SNAT activity only at the highest dose (1 microM) whereas PGF2 alpha, 15-ket...
journal_title:Molecular and cellular endocrinology
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doi:10.1016/0303-7207(81)90066-6
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
doi:10.1016/j.mce.2014.09.019
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章,评审
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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更新日期:2015-01-05 00:00:00
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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更新日期:2011-01-01 00:00:00
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
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journal_title:Molecular and cellular endocrinology
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更新日期:2008-01-30 00:00:00
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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更新日期:1980-07-01 00:00:00
abstract::In the extracellular space, the gonadotropin-releasing hormone (GnRH) is metabolized by the zinc metalloendopeptidase EC3.4.24.15 (EP24.15) to form the pentapeptide, GnRH-(1-5). GnRH-(1-5) diverges in function and mechanism of action from GnRH in the brain and periphery. GnRH-(1-5) acts on the orphan G protein-coupled...
journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
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更新日期:2015-11-05 00:00:00
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
doi:10.1016/0303-7207(79)90015-7
更新日期:1979-02-01 00:00:00