Identification of Inducible Genes at the Early Stage of Adipocyte Differentiation of 3T3-L1 Cells

1999 ◽  
Vol 254 (2) ◽  
pp. 299-305 ◽  
Author(s):  
Masayoshi Imagawa ◽  
Tomoko Tsuchiya ◽  
Tsutomu Nishihara
Keyword(s):  
Adipocyte Differentiation ◽  
Early Stage ◽  
Inducible Genes

Induction of Bach1 and ARA70 gene expression at an early stage of adipocyte differentiation of mouse 3T3-L1 cells

2002 ◽  
Vol 361 (3) ◽  
pp. 629-633 ◽  
Author(s):  
Makoto NISHIZUKA ◽  
Tomoko TSUCHIYA ◽  
Tsutomu NISHIHARA ◽  
Masayoshi IMAGAWA
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
3T3 Cells ◽  
Subtraction Method ◽  
Proliferating Cells ◽  
Genes Encoding ◽  
Nih 3T3

Using a subtraction method, we have isolated genes that are induced early in the differentiation of mouse 3T3-L1 preadipocyte cells into adipocytes. These include the genes encoding transcription factors and signalling proteins, as well as unknown genes. Bach1, a transcription factor, and ARA70, a cofactor, were rapidly induced during differentiation. The induction of these two genes was observed only in growth-arrested 3T3-L1 cells, and not in proliferating cells. In NIH-3T3 cells, no induction was observed under either set of conditions. These results strongly indicate that Bach1 and ARA70 have valuable roles at the onset of adipocyte differentiation.

Dicer has a crucial role in the early stage of adipocyte differentiation, but not in lipid synthesis, in 3T3-L1 cells

2012 ◽  
Vol 420 (4) ◽  
pp. 931-936 ◽  
Author(s):  
Yuri Fujimoto ◽  
Yoshimi Nakagawa ◽  
Akiko Shingyouchi ◽  
Naoko Tokushige ◽  
Noriko Nakanishi ◽  
...  
Keyword(s):  
Crucial Role ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Lipid Synthesis

scholarly journals Regulation of Adipose Differentiation by Fructose and GluT5

2012 ◽  
Vol 26 (10) ◽  
pp. 1773-1782 ◽  
Author(s):  
Li Du ◽  
Anthony P. Heaney
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Whole Body ◽  
Wild Type ◽  
Embryonic Fibroblasts ◽  
Fructose Intake ◽  
Adipose Differentiation

Abstract Adipose tissue is an important metabolic organ that is crucial for whole-body insulin sensitivity and energy homeostasis. Highly refined fructose intake increases visceral adiposity although the mechanism(s) remain unclear. Differentiation of preadipocytes to mature adipocytes is a highly regulated process that is associated with characteristic sequential changes in adipocyte gene expression. We demonstrate that fructose treatment of murine 3T3-L1 cells incubated in standard differentiation medium increases adipogenesis and adipocyte-related gene expression. We further show that the key fructose transporter, GluT5, is expressed in early-stage adipocyte differentiation but is not expressed in mature adipocytes. GluT5 overexpression or knockdown increased and decreased adipocyte differentiation, respectively, and treatment of 3T3-L1 cells with a specific GluT5 inhibitor decreased adipocyte differentiation. Epidymal white adipose tissue was reduced in GluT5−/− mice compared with wild-type mice, and mouse embryonic fibroblasts derived from GluT5−/− mice exhibited impaired adipocyte differentiation. Taken together, these results demonstrate that fructose and GluT5 play an important role in regulating adipose differentiation.

Expression of p68 RNA Helicase Is Closely Related to the Early Stage of Adipocyte Differentiation of Mouse 3T3-L1 Cells

2001 ◽  
Vol 287 (2) ◽  
pp. 435-439 ◽  
Author(s):  
Atsushi Kitamura ◽  
Makoto Nishizuka ◽  
Kei Tominaga ◽  
Tomoko Tsuchiya ◽  
Tsutomu Nishihara ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Early Stage ◽  
Rna Helicase ◽  
P68 Rna Helicase

scholarly journals MYOD1 Inhibits Avian Adipocyte Differentiation via miRNA-206/KLF4 Axis

2020 ◽  
Author(s):  
Zheng Wang ◽  
Qiang-Sen Zhao ◽  
Xiao-Qin Li ◽  
Zhong-Tao Yin ◽  
Si-Rui Chen ◽  
...  
Keyword(s):  
Body Fat ◽  
Target Gene ◽  
Muscle Development ◽  
Potential Role ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Fat Distribution ◽  
Inhibitory Effect ◽  
Over Expression ◽  
Klf4 Expression

Abstract Background: A considerable number of muscle development-related genes were differentially expressed in the early stage of avian adipocyte differentiation. However, the functions of them in adipocyte differentiation remain largely known. In this study, the myoblast determination protein 1 (MYOD1) was selected as a representative of muscle development and we investigated its expression, function and regulation in avian adipocyte differentiation.Results: The expression of MYOD1 decreased significantly in the early stage of avian adipocyte differentiation. CRISPR/CAS9-mediated deletion of MYOD1 induced adipocyte differentiation, whereas over-expression of MYOD1 inhibited adipogenesis. mRNA-seq showed that MYOD1 could perturb the lipid biosynthetic process during differentiation. Mechanistically, MYOD1 directly up-regulates the miR-206 expression by binding upstream 1200 bp region, and over-expression of miR-206 also inhibits adipogenesis. Furthermore, MYOD1 affected the expression of endogenous miR-206 and its target gene Kruppel Like Factor 4 (KLF4), which is an important activator of adipogenesis. Accordingly, the inhibition of miR-206 or over-expression of KLF4 could counteract the inhibitory effect of MYOD1 on adipocyte differentiation. Conclusions: These findings suggest that MYOD1 inhibited adipocyte differentiation by up-regulating miR-206 to suppress the KLF4 expression. Collectively, these findings identify a novel function of MYOD1 in adipocyte differentiation, suggesting a potential role in body-fat distribution regulation.

scholarly journals Anti-adipogenic Activity of Cordyceps militaris in 3T3-L1 Cells

2011 ◽  
Vol 6 (12) ◽  
pp. 1934578X1100601 ◽  
Author(s):  
Qing Liu ◽  
In Pyo Hong ◽  
Mi-Jeong Ahn ◽  
Hwan-Soo Yoo ◽  
Sang-Bae Han ◽  
...  
Keyword(s):  
Inhibitory Activity ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Cordyceps Militaris ◽  
Active Compounds ◽  
Fat Accumulation ◽  
Combinational Treatment ◽  
Treatment Of Obesity ◽  
Oil Red O Staining ◽  
Oil Red O

Inhibition of adipocytes differentiation is suggested to be an important strategy for prevention and/or treatment of obesity. In our present study, Cordyceps militaris showed significant inhibitory activity on adipocyte differentiation in 3T3-L1 preadipocytes as assessed by measuring fat accumulation using Oil Red O staining. Activity-guided fractionation led to the isolation of cordycepin (1), guanosine (2) and tryptophan (3) as active compounds. All the three compounds were more effective in the prevention of early stage of adipogenesis than in lipolysis. In addition, combinational treatment of three compounds significantly increased anti-adipogenic activity.

scholarly journals Lignan from Alnus japonica Inhibits Adipocyte Differentiation via Cell Cycle and FOXO1 Regulation

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3346
Author(s):  
Hyejin Lee ◽  
Ji Hye Jeong ◽  
Jae-Ha Ryu
Keyword(s):  
Cell Cycle ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Inhibitory Effect ◽  
Alnus Japonica ◽  
Akt Phosphorylation ◽  
Cycle Arrest ◽  
Forkhead Box ◽  
Mitotic Clonal Expansion

In the present study, we isolated a lignan ((−)-(2R,3R)-1,4-O-diferuloylsecoisolariciresinol, DFS) from Alnus japonica and evaluated its antiobesity potential in vitro. We also determined its mechanism of action in a mouse pre-adipocyte 3T3-L1 cell line. DFS dose- and day-dependently inhibited adipogenesis by downregulation of adipogenic factors and lipid metabolism-regulating factors during adipocyte differentiation. In particular, DFS suppressed cell cycle-regulating factors and induced G0/G1 cell cycle arrest, implying that it had an inhibitory effect on mitotic clonal expansion which occurred at an early stage of adipogenesis. DFS also suppressed adipogenesis through decreasing Akt phosphorylation and increasing the level of Forkhead box protein-O1 (FOXO1). These results suggest that DFS may be a pharmacological candidate for the development of antiobesity, therapeutic, and nutraceutical products.

scholarly journals Inhibitory Effects of Hwangryunhaedok-Tang in 3T3-L1 Adipogenesis by Regulation of Raf/MEK1/ERK1/2 Pathway and PDK1/Akt Phosphorylation

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Dong Hoon Kwak ◽  
Ji-Hye Lee ◽  
Dong-Gun Kim ◽  
Taesoo Kim ◽  
Kwang Jin Lee ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Protein Kinase ◽  
High Performance ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Mitogen Activated Protein Kinase ◽  
Inhibitory Effects ◽  
Akt Phosphorylation ◽  
Enhancer Binding Protein ◽  
Mitogen Activated Protein

Hwangryunhaedok-tang (HRT) has been long used as traditional medicine in Asia. However, inhibitory role of HRT is unclear in early stage of 3T3-L1 adipocyte differentiation related to signaling. In the present study, we investigated the inhibitory effects of HRT on upstream signaling of peroxisome proliferation-activity receptor-γ(PPAR-γ) and CCAAT/enhancer binding protein-β(C/EBP-β) expression in differentiation of 3T3-L1 preadipocytes. We found that HRT significantly inhibited the adipocyte differentiation by downregulating several adipocyte-specific transcription factors including PPAR-γ, C/EBP-α, and C/EBP-βin 3T3-L1 preadipocytes. Furthermore, we observed that HRT markedly inhibited the differentiation media-mediated phosphorylation of Raf/extracellular mitogen-activated protein kinase 1 (MEK1)/signal-regulated protein kinase 1/2 (ERK1/2) and phosphorylation of phosphoinositide-dependent kinase 1 (PDK1)/Akt. These results indicate that anti-adipogenesis mechanism involves the downregulation of the major transcription factors of adipogenesis including PPAR-γand C/EBP-αthrough inhibition of Raf/MEK1/ERK1/2 phosphorylation and PDK1/Akt phosphorylation by HRT. Furthermore, high performance liquid chromatography (HPLC) analysis showed HRT contains active antiobesity constituents such as palmatine, berberine, geniposide, baicalin, baicalein, and wogonin. Taken together, this study suggested that anti-adipogenesis effects of HRT were accounted by downregulation of Raf/MEK1/ERK1/2 pathway and PDK1/Akt pathway during 3T3-L1 adipocyte differentiation.

Regulation of adipocyte differentiation of 3T3-L1 cells by PDZRN3

2013 ◽  
Vol 304 (11) ◽  
pp. C1091-C1097 ◽  
Author(s):  
Takeshi Honda ◽  
Aiko Ishii ◽  
Makoto Inui
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Adipogenic Differentiation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Protein Levels ◽  
Upstream Regulator ◽  
Pparγ Expression

PDZRN3, a member of the PDZRN (or LNX) family of proteins, is essential for the differentiation of mesenchymal stem cells into myotubes, but it plays an inhibitory role in the differentiation of these cells into osteoblasts. Given that mesenchymal stem cells also differentiate into adipocytes, we examined the possible role of PDZRN3 in adipogenesis in mouse 3T3-L1 preadipocytes. The expression of PDZRN3 decreased at both the mRNA and protein levels during adipogenic differentiation. RNAi-mediated depletion of PDZRN3 enhanced the differentiation of 3T3-L1 cells into adipocytes as assessed on the basis of lipid accumulation. The upregulation of aP2 and CCAAT/enhancer-binding protein (C/EBP)-β during adipocyte differentiation was also enhanced in the PDZRN3-depleted cells, as was the induction of peroxisome proliferator-activated receptor-γ (PPARγ), an upstream regulator of aP2 and C/EBPα, at both the mRNA and protein levels. Among transcription factors that control the expression of PPARγ, we found that STAT5b, but not STAT5a, was upregulated in PDZRN3-depleted cells at both mRNA and protein levels. Tyrosine phosphorylation of STAT5b, but not that of STAT5a, was also enhanced at an early stage of differentiation by PDZRN3 depletion. In addition, the expression of C/EBPβ during the induction of differentiation was enhanced at the mRNA and protein levels in PDZRN3-depleted cells. Our results thus suggest that PDZRN3 negatively regulates adipogenesis in 3T3-L1 cells through downregulation of STAT5b and C/EBPβ and consequent suppression of PPARγ expression.

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