• 제목/요약/키워드: Brown adipocytes

검색결과 34건 처리시간 0.026초

Effect of Thyroid hormone on Lipogenesis in Rat White and Brown Adipocytes Culture System

  • Kim, Yangha -Moon
    • Preventive Nutrition and Food Science
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    • 제3권4호
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    • pp.362-367
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    • 1998
  • Thyroid hormone(T3) stimulates hepatic lipogenesis by increasing expression of genes, indluding acetyl-CoA carboxylase and fatty acid synthase. S14 protein, which is thougth to be involved in lipid metabolism , appears to respond in parallel . Effect of T3 on lipogenesis in white and brown adipose tissue are less clear, and may be complicated by indirect effects of the hormone. We developed an adipocytes system where the indirect effects of thyroid hormone are abolished and direct effects of T3 on lipogenesis could be tested. Fat accumulation was mesured by Oil-Red O staining. Insulin clearly enhanced fat accumulation by 2-fold . Isobutylemethylxanthie(IBMX) apeared to inhibit insulin -stimulated fat accumulation. Dexamethasone increased insulin-stimulatedfat accumulation about 1.3-fold. confluent adipocytes were cultured in serum-free medium or medium containing 10% fetal calf serum or 10% fetal calf serum stripped of thyroid hormone and lipogenesis, assessed by the incorporation of 3H2O , was measured. Medium without serum or supplemented with T3-depleted serum did not amplify the stimulatory effect of T3 on lipogenesis compared to medium containing 10% fetal calf seru. Dexamethasone alone led to a decrease inlopogenesis of about 50 % in white adipocytes and 25% in brown adipocytes. However, dexamethasone amplified the lipogenic respnse to T3 by about 30% in whit eadipocytes and 60% in brown adipocytes. T3(1$\mu$M) stimulated lipogenesis and acetyl-CoA carboxylase and fatty acid syntase mRNA levels up to 2 -fold in both types of adipocytes. It seems that these adipocytes systems are as useful model to study the effects of hormones on lipogenic gene expression as well as lipogenesis.

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High-fat diet alters the thermogenic gene expression to β-agonists or 18-carbon fatty acids in adipocytes derived from the white and brown adipose tissue of mice

  • Seonjeong Park;Seung A Ock;Yun Jeong Park;Yoo-Hyun Lee;Chan Yoon Park;Sunhye Shin
    • Journal of Nutrition and Health
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    • 제57권2호
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    • pp.171-184
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    • 2024
  • Purpose: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and related metabolic disorders, emerging evidence suggests that it is difficult to induce adipocyte thermogenesis in obesity. Therefore, this study aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity. Methods: Adipose progenitor cells were isolated from the white and brown adipose tissues of control diet (CD) or high-fat diet (HFD) fed mice, and fully differentiated white and brown adipocytes were treated with β-agonists or 18-carbon fatty acids for β-adrenergic activation or peroxisome proliferator-activated receptor (PPAR) activation. Results: Compared to the CD-fed mice, the expression of uncoupling protein 1 (Ucp1) was lower in the white adipose tissue of the HFD-fed mice; however, this was not observed in the brown adipose tissue. The expression of peroxisome proliferator-activated receptor gamma (Pparg) was lower in the brown adipose progenitor cells isolated from HFD-fed mice than in those isolated from the CD-fed mice. Norepinephrine (NE) treatment exerted lesser effect on peroxisome proliferator-activated receptor-γ coactivator (Pgc1a) upregulation in white adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, the expression levels of thermogenic genes including Ucp1, Pgc1a, and positive regulatory domain zinc finger region protein 16 (Prdm16) were higher in the white adipocytes derived from HFD-fed mice. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white adipocytes derived from HFD-fed mice. Brown adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Conclusion: These results indicate that diet-induced obesity may downregulate brown adipogenesis and NE-induced thermogenesis in white adipocytes. Also, HFD feeding may induce thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA could augment the expression levels.

발아현미가 LPS로 유도된 지방세포의 염증반응에 미치는 영향 (Effect of Germinated Brown Rice on LPS-Induced Inflammation in Adipocytes)

  • 박미영
    • 한국식생활문화학회지
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    • 제33권4호
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    • pp.337-344
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    • 2018
  • Germinated brown rice (GBR, Orysa sartiva L.) has been reported to have anti-obesity and anti-inflammatory effects. However, the mechanisms underlying these effects in adipocytes are not fully understood. Therefore, this study was conducted to explore the anti-inflammatory mechanisms of GBR on lipopolysaccharide (LPS)-stimulated 3T3-L1 adipocytes. 3T3-L1 adipocytes were pretreated with GBR extracts (0-20 mg/mL) 1 h before LPS stimulation. The mRNA expression of adipokines and Toll-like receptor 4 (TLR4) were measured by RT-PCR. The protein expressions of TLR4-related molecules were detected by western blotting and nuclear factor-${\kappa}B$ ($NF-{\kappa}B$) activation was measured. Our results showed that GBR extract dose-dependently inhibited mRNA expression of LPS-induced tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1). GBR extract was found to inhibit LPS-induced mRNA expression of TLR4 and protein expression of both myeloid differentiation factor 88 (MyD88) and TNF receptor-associated factor 6 (TRAF6). Furthermore, GBR extract significantly inhibited extracellular receptor-activated kinase (ERK) phosphorylation and $NF-{\kappa}B$ activation. These results suggest that GBR extract has the anti-inflammatory effects on LPS-induced inflammation via inhibition of TLR4 signaling, includingthe ERK and $NF-{\kappa}B$ signaling pathways, in adipocytes.

Medicarpin induces lipolysis via activation of Protein Kinase A in brown adipocytes

  • Imran, Khan Mohammad;Yoon, Dahyeon;Lee, Tae-Jin;Kim, Yong-Sik
    • BMB Reports
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    • 제51권5호
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    • pp.249-254
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    • 2018
  • Natural pterocarpan Medicarpin (Med) has been shown to have various beneficial biological roles, including inhibition of osteoclastogenesis, stimulation of bone regeneration and induction of apoptosis. However, the effect of the Med on lipolysis in adipocytes has not been reported. Here, we show the effect of Med on lipolysis in different mouse adipocytes and elucidate the underlying mechanism. We observed that Med treatment promoted release of glycerol in the media. Differentiated mouse brown adipose tissue cells were treated with Med. RNA-Seq analysis was performed to elucidate the effect of med and subsequently was confirmed by qRT-PCR and western blotting analyses. Med treatment increased both protein and gene expression levels of hormone-sensitive lipase (Hsl) and adipose triglyceride lipase (Atgl), which are two critical enzymes necessary for lipolysis. Mechanistic study showed that Med activates Protein Kinase A (PKA) and phosphorylates Hsl at PKA target position at $Serine^{660}$. Silencing of PKA gene by short interfering RNA attenuated the Med-induced increase in glycerol release and Hsl phosphorylation. The results unveil that Med boosts lipolysis via a PKA-dependent pathway in adipocytes and may provide a possible avenue of further research of Med mediated reduction of body fat.

Evaluation of the inhibition of the differentiation of pre-adipocytes into matures adipocytes

  • Morvan, Pierre Yves
    • 대한화장품학회:학술대회논문집
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    • 대한화장품학회 2003년도 IFSCC Conference Proceeding Book I
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    • pp.440-447
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    • 2003
  • Up until today, the key to contouring has been resumed in these two alternatives, either limiting the adipocyte storing capacity by modulating lipogenesis, or by stimulating lipolysis to eliminate adipocyte lipid content. Another interesting way could be the regulation of adipocyte differentiation. In this work, we have evaluated the effect of a brown algal extract of Sphacelaria scoparia (SSE) on the differentiation of pre-adipocytes into adipocytes. A pre-adipocyte line (3T3-L 1) was used. The differentiation was evaluated by the measure of produced lipids thanks to red oil coloration and spectrophotometry, and also by the expression of adipocyte differentiation markers: enzymes such as fatty acid synthase (FAS) and stearoyl CoA desaturase (SCD), or membrane proteins such as glucose transporters (GLUT -4) and fatty acid transporters (FAT) expressed on the surface of human adipocytes. These genes are under control of two transcription factors: CAAT-enhancer binding protein (c/EBP alpha) and sterol response element binding protein (SREBP1). All these markers were analysed at different stages of differentiation by RT -PCR. Sphacelaria extract (SSE) inhibits pre-adipocytes differentiating into adipocytes following a dose-dependant relation, using a kinetics similar to retinoic acid. It decreases the expression of mRNA specific to FAS, FAT, GLUT -4, SCD1, c/EBP alpha and SREBP1. Moreover, SSE regulated on collagen 1 and collagen 4 expression. A stimulation of collagen 1 was also measured in human skin fibroblasts. Thus, SSE performs as a genuine differentiation inhibitor and not only as a lipogenesis inhibitor, and could be used in slimming products.

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Protein Tyrosine Phosphatase, Receptor Type B (PTPRB) Inhibits Brown Adipocyte Differentiation through Regulation of VEGFR2 Phosphorylation

  • Kim, Ji Soo;Kim, Won Kon;Oh, Kyoung-Jin;Lee, Eun-Woo;Han, Baek Soo;Lee, Sang Chul;Bae, Kwang-Hee
    • Journal of Microbiology and Biotechnology
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    • 제29권4호
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    • pp.645-650
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    • 2019
  • Brown adipocytes have an important role in the regulation of energy balance through uncoupling protein-1 (UCP-1)-mediated nonshivering thermogenesis. Although brown adipocytes have been highlighted as a new therapeutic target for the treatment of metabolic diseases, such as obesity and type II diabetes in adult humans, the molecular mechanism underlying brown adipogenesis is not fully understood. We recently found that protein tyrosine phosphatase receptor type B (PTPRB) expression dramatically decreased during brown adipogenic differentiation. In this study, we investigated the functional roles of PTPRB and its regulatory mechanism during brown adipocyte differentiation. Ectopic expression of PTPRB led to a reduced brown adipocyte differentiation by suppressing the tyrosine phosphorylation of VEGFR2, whereas a catalytic inactive PTPRB mutant showed no effects on differentiation and phosphorylation. Consistently, the expression of brown adipocyte-related genes, such as UCP-1, $PGC-1{\alpha}$, PRDM16, $PPAR-{\gamma}$, and CIDEA, were significantly inhibited by PTPRB overexpression. Overall, these results suggest that PTPRB functions as a negative regulator of brown adipocyte differentiation through its phosphatase activity-dependent mechanism and may be used as a target protein for the regulation of obesity and type II diabetes.

Effect of Solid-State Fermented Brown Rice Extracts on 3T3-L1 Adipocyte Differentiation

  • Su Bin Ji;Chae Hun Ra
    • Journal of Microbiology and Biotechnology
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    • 제33권7호
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    • pp.926-933
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    • 2023
  • Aspergillus oryzae KCCM 11372 was used to enhance the production of β-glucan using humidity control strategies. Under conditions of 60% humidity, solid-state fermentation (SSF) increased the yields of enzymes (amylase and protease), fungal biomass (ergosterol), and β-glucan. The maximum concentrations obtained were 14800.58 U/g at 72 h, 1068.14 U/g at 120 h, 1.42 mg/g at 72 h, and 12.0% (w/w) at 72 h, respectively. Moreover, the β-glucan containing fermented brown rice (β-glucan-FBR) extracts at concentrations of 25-300 ㎍/ml was considered noncytotoxic to 3T3-L1 preadipocytes. We then studied the inhibitory effects of the extracts on fat droplet formation in 3T3-L1 cells. As a result, 300 ㎍/ml of β-glucan-FBR extracts showed a high inhibition of 38.88% in lipid accumulation. Further, these extracts inhibited adipogenesis in the 3T3-L1 adipocytes by decreasing the expression of C/EBPα, PPARγ, aP2, and GLUT4 genes.

Construction and Characterization of Novel Expression Vectors for Genetic Adipose Tissue Ablation

  • Ko, Duck Sung;Choi, Woong Hwan;Kim, Chul Geun
    • Animal cells and systems
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    • 제2권2호
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    • pp.249-258
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    • 1998
  • Obesity, one of the most common metabolic diseases in industrial countries is characterized by an increase in the number or size of adipocytes. In an effort to create transgenic mouse models for the study of obesity we developed a novel technique in which adipose tissue can be ablated genetically at will, at any specific developmental stage and/or physiological condition, by the treatment of ganciclovir. We made a series of adipocytespecific expression vectors using minimal regulatory regions of brown adipocyte-specific uncoupling protein (UCP-1) gene and adipocyte-specific aP2 gene, and then analyzed their expression characteristics in cultured cell lines. When both constructs pUCP-LacZ and paP2-LacZ were transfected transiently into differentiating 3T3-L1 (pre-while adipocytes) and HIB-1B (pre-brown adipocytes) cell lines in vitro and then monitored by X-gal staining of cells, these regulatory regions were sufficient to show proper differentiation stage-specific expression in adipocvtes. To confirm that adipocytes expressing HSV-TK controlled by these minimal requlatory elements are sufficient to kill themselves with ganciclovir treatment pUCP-TK and paP2-TK expression constructs were transfected stably into HIB-1B and 3T3-L1 cells, respectively, and their ganciclovir sensitivities were tested during in vitro differentiation of cells. As expected more than 80% of cells were dead by the 7th day of treatment with ganciclovir while negative control cells were not affected at all. The data suqqest that the constructed vectors are suitable for obtaining novel obese transqenic models based on a conditional genetic tissue ablation method.

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후코이단의 3T3-L1 지방세포에서 PI3K/AMPK 경로를 통한 포도당 흡수 촉진 및 인슐린 민감성 증진 효과 (Fucoidan Stimulates Glucose Uptake via the PI3K/AMPK Pathway and Increases Insulin Sensitivity in 3T3-L1 Adipocytes)

  • 이지희;박재은;한지숙
    • 생명과학회지
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    • 제31권1호
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    • pp.1-9
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    • 2021
  • 본 연구는 갈조류 유래 물질인 후코이단이 인슐린 민감성을 증진시키는지를 규명하기 위하여 3T3-L1 지방세포에서 포도당 흡수에 미치는 후코이단의 영향을 측정하고 그 작용기전을 조사하였다. 후코이단은 지방세포에서 포도당 흡수를 유의하게 증가시켰으며 이는 PM-GLUT4의 발현 증가와 관련이 있음을 관찰하였다. 후코이단은 인슐린 신호전달 경로에서 PI3K의 활성화 및 pIRS1tyr, Akt, PKCλ/ζ의 인산화를 대조군에 비해 유의하게 증가시켰다. 또한, AMPK의 활성화를 나타내는 pAMPK 수준이 유의하게 증가하였다. 이들 PI3K 및 AMPK 활성화는 포도당 수송체인 GLUT4를 세포막으로 이동시켰으며 이로 인하여 PM-GLUT4의 발현이 증가되고 포도당 흡수가 촉진되었다. 후코이단에 의한 PI3K 및 AMPK 경로의 활성화를 증명하기 위해, PI3K 억제제인 Wortmannin과 AMPK의 억제제인 Compound C를 사용하여 이들 처리에 의한 포도당 흡수능과 PM-GLUT4의 발현을 측정한 결과 이들의 발현이 유의하게 저해되었다. 따라서 후코이단은 3T3-L1 지방세포에서 PI3K 및 AMPK 경로를 활성화시킴으로써 인슐린 민감성을 증진하고 포도당 흡수를 촉진시킬 수 있음을 나타내었다.