Proteomic analysis for inhibitory effect of chitosan oligosaccharides on 3T3-L1 adipocyte differentiation

PROTEOMICS ◽  
2008 ◽  
Vol 8 (3) ◽  
pp. 569-581 ◽  
Author(s):  
Md. Atiar Rahman ◽  
Suresh G. Kumar ◽  
Sang Woo Kim ◽  
Hye Jin Hwang ◽  
Yu Mi Baek ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Adipocyte Differentiation ◽  
Inhibitory Effect ◽  
Chitosan Oligosaccharides

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

2006 ◽  
Vol 290 (2) ◽  
pp. E273-E281 ◽  
Author(s):  
Hang-Seng Liu ◽  
Yen-Hang Chen ◽  
Pei-Fang Hung ◽  
Yung-Hsi Kao
Keyword(s):  
Green Tea ◽  
Adipocyte Differentiation ◽  
Epigallocatechin Gallate ◽  
Inhibitory Effect ◽  
Mrna Levels ◽  
Erk Pathway ◽  
Extracellular Signal ◽  
Basal Half ◽  
The Stability ◽  
New Protein

Resistin (Rstn) is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. By contrast, green tea catechins, especially (−)-epigallocatechin gallate (EGCG), have been reported as body weight and diabetes chemopreventatives. Whether EGCG regulates production of Rstn is unknown. Using 3T3-L1 adipocytes, we found that EGCG at 20 and 100 μM suppressed Rstn mRNA levels by ∼35 and 50%, respectively, after 3 h. The basal half-life of Rstn mRNA induced by actinomycin D was >12 h but shifted to 3 h in the presence of EGCG. This suggests that EGCG regulates the stability of Rstn mRNA. Treatment with cycloheximide did not prevent EGCG-suppressed Rstn mRNA levels, which suggests that the effect of EGCG does not require new protein synthesis. Intracellular Rstn protein significantly decreased in the presence of 100 μM EGCG 3 h after treatment, whereas the release of the Rstn protein did not significantly change. This suggests that EGCG may modulate the distribution of Rstn protein between the intracellular and extracellular compartments. EGCG did not affect the amounts of extracellular signal-related kinase-1/2 (ERK1/2), phospho-JNK, phospho-p38, and phospho-Akt proteins but reduced the amounts of phospho-ERK1/2 proteins. Overexpression with MEK1 blocked EGCG-inhibited Rstn mRNA expression. These data suggest that EGCG downregulates Rstn expression via a pathway that is dependent on the ERK pathway.

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 Fermentation characteristics and inhibitory effect of brown rice vinegar on adipocyte differentiation in 3T3-L1 cells

2021 ◽  
Vol 28 (3) ◽  
pp. 416-425
Author(s):  
Eun Ah Sim ◽  
Hyeon Hwa Oh ◽  
Do Youn Jeong ◽  
Geun-Seoup Song ◽  
Young-Soo Kim
Keyword(s):  
Adipocyte Differentiation ◽  
Brown Rice ◽  
Inhibitory Effect ◽  
Rice Vinegar

scholarly journals A novel peptide RIFV suppresses human adipocyte differentiation through the inhibition of C/EBP-β expression

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Wen Zhang ◽  
Dan Shen ◽  
Yun Li ◽  
Hong Zhong ◽  
Xing Wang ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Epidemic Disease ◽  
Global Epidemic ◽  
Protein Levels ◽  
Therapeutic Drugs ◽  
Peptide Database ◽  
Gene Assay

Abstract Background Obesity is a global epidemic disease that increases the risk of metabolic syndrome. However, therapeutic drugs for obesity are still scarce. In recent years, peptides have been identified as new biological regulators. RIFV (R-I-F-V-P-I-K-G-R-P-A-P), a novel active peptide from our peptide database. Methods We performed oil red O staining and triglyceride measurement to analyze the influence of RIFV on white preadipocytes differentiation. Then the effects of RIFV on cell proliferation, apoptosis and cell cycle were determined by using CCK-8 assay and flow cytometry. The mRNA and protein levels of adipogenesis-related genes were respectively detected by qRT-PCR and western blot. Rescue experiment was conducted to confirm whether RIFV could regulate adipocytes differentiation via targeting C/EBP-β. Finally, the luciferase reporter gene assay was performed to verify the regulation of RIFV on C/EBP-β gene. Results RIFV was revealed to inhibit the differentiation of human white adipocytes without affecting their proliferation. Additionally, RIFV could also suppress the differentiation of mouse primary white preadipocytes isolated from inguinal fat tissues. Furthermore, RIFV may have an inhibitory effect on adipogenesis by inhibiting the regulation of the adipogenic gene C/EBP-β. Conclusions Our results indicated that RIFV may be a novel essential regulator of adipocyte differentiation and represents a therapeutic strategy for obesity and related complications.

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.

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