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Adipocyte Differentiation (adipocyte + differentiation)
Selected AbstractsDisruption of hepatic adipogenesis is associated with impaired liver regeneration in miceHEPATOLOGY, Issue 6 2004Eyal Shteyer The liver responds to injury with regulated tissue regeneration. During early regeneration, the liver accumulates fat. Neither the mechanisms responsible for nor the functional significance of this transient steatosis have been determined. In this study, we examined patterns of gene expression associated with hepatic fat accumulation in regenerating liver and tested the hypothesis that disruption of hepatic fat accumulation would be associated with impaired hepatic regeneration. First, microarray-based gene expression analysis revealed that several genes typically induced during adipocyte differentiation were specifically upregulated in the regenerating liver prior to peak hepatocellular fat accumulation. These observations suggest that hepatic fat accumulation is specifically regulated during liver regeneration. Next, 2 methods were employed to disrupt hepatocellular fat accumulation in the regenerating liver. Because exogenous leptin supplementation reverses hepatic steatosis in leptin-deficient mice, the effects of leptin supplementation on liver regeneration in wild-type mice were examined. The data showed that leptin supplementation resulted in suppression of hepatocellular fat accumulation and impairment of hepatocellular proliferation during liver regeneration. Second, because glucocorticoids regulate cellular fat accumulation during adipocyte differentiation, the effects of hepatocyte-specific disruption of the glucocorticoid receptor were similarly evaluated. The results showed that hepatic fat accumulation and hepatocellular proliferation were also suppressed in mice with liver specific disruption of glucocorticoid receptor. In conclusion, suppression of hepatocellular fat accumulation is associated with impaired hepatocellular proliferation following partial hepatectomy, indicating that hepatocellular fat accumulation is specifically regulated during and may be essential for normal liver regeneration. (HEPATOLOGY 2004;40:1322,1332.) [source] Correlation between the high expression of C/EBP, protein in F442A cells and their relative resistance to antiadipogenic action of TCDD in comparison to 3T3-L1 cellsJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2002Phillip C. C. Liu Abstract We compared the ability of two clonally derived murine preadipocyte cell lines, 3T3-L1(L1) and 3T3-F442A (F442A), to differentiate after treatment by 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), and found that the former cell line was clearly suppressed by TCDD but the latter was not. It was initially postulated that the easiest way to explain the lack of response to TCDD in F442A cells could be an alteration in aryl hydrocarbon receptor (AhR) functionality. This hypothesis was tested first, but no differences were found in the levels or functions of AhR. To find an alternate explanation for such a differential effect of TCDD, we tested the action of several diagnostic agents on the process of adipocyte differentiation of these two cells. No differences were found between these two lines of cells in the susceptibility to the antiadipogenic action of 12-0-tetradecanoylphorbol-13-acetate (TPA), or to TNF,, indicating that the basic biochemical components engaged in the antiadipogenic actions of these agents in these two cell lines are similar. In contrast, F442A cells were found to be more resistant to the antiadipogenic action of EGF or TGF, than L1 cells which were tested side by side. Based on the knowledge that TNF, preferentially affects C/EBP, and that TGF, specifically controls C/EBP, and , in their antiadipogenic action, we hypothesized that the major cause for the differential response of these two similar cell lines could be the insensitivity of C/EBP, and/or , of F442A cells to the action of TCDD. We could obtain supporting data for this hypothesis, showing that in F442A cells, the level of C/EBP, is already high even before the addition of adipocyte differentiation factors and that TCDD did not cause any significant changes in the titer of C/EBP,. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:70,83, 2002; Published online in Wiley Interscience (www.interscience.wiley.com). DOI 10.1002/jbt.10020 [source] Krüppel-Like Zinc Finger Protein Glis3 Promotes Osteoblast Differentiation by Regulating FGF18 Expression,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2007Ju Youn Beak Abstract The zinc finger protein Glis3 is highly expressed in human osteoblasts and acts synergistically with BMP2 and Shh in enhancing osteoblast differentiation in multipotent C3H10T1/2 cells. This induction of osteoblast differentiation is at least in part caused by the induction of FGF18 expression. This study supports a regulatory role for Glis3 in osteoblast differentiation. Introduction: Gli-similar 3 (Glis3) is closely related to members of the Gli subfamily of Krüppel-like zinc finger proteins, transcription factors that act downstream of sonic hedgehog (Shh). In this study, we analyzed the expression of Glis3 in human osteoblasts and mesenchymal stem cells (MSCs). Moreover, we examined the regulatory role of Glis3 in the differentiation of multipotent C3H10T1/2 cells into osteoblasts and adipocytes. Materials and Methods: Microarray analysis was performed to identify genes regulated by Glis3 in multipotent C3H10T1/2 cells. Reporter and electrophoretic mobility shift assays were performed to analyze the regulation of fibroblast growth factor 18 (FGF18) by Glis3. Results: Glis3 promotes osteoblast differentiation in C3H10T1/2 cells as indicated by the induction of alkaline phosphatase activity and increased expression of osteopontin, osteocalcin, and Runx2. In contrast, Glis3 expression inhibits adipocyte differentiation. Glis3 acts synergistically with BMP2 and Shh in inducing osteoblast differentiation. Deletion analysis indicated that the carboxyl-terminal activation function of Glis3 is needed for its stimulation of osteoblast differentiation. Glis3 is highly expressed in human osteoblasts and induced in MSCs during differentiation along the osteoblast lineage. Microarray analysis identified FGF18 as one of the genes induced by Glis3 in C3H10T1/2 cells. Promoter analysis and electrophoretic mobility shift assays indicated that a Glis3 binding site in the FGF18 promoter flanking region is important in its regulation by Glis3. Conclusions: Our study showed that Glis3 positively regulates differentiation of C3H10T1/2 cells into osteoblasts and inhibits adipocyte differentiation. Glis3 acts synergistically with BMP2 and Shh in inducing osteoblast differentiation. The promotion of osteoblast differentiation by Glis3 involves increased expression of FGF18, a positive regulator of osteogenesis. This, in conjunction with the induction of Glis3 expression during osteoblast differentiation in MSCs and its expression in osteoblasts, suggests that Glis3 is an important modulator of MSC differentiation. [source] Regulation of Human Skeletal Stem Cells Differentiation by Dlk1/Pref-1JOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2004Basem M Abdallah Abstract Dlk-1/Pref-1 was identified as a novel regulator of human skeletal stem cell differentiation. Dlk1/Pref-1 is expressed in bone and cultured osteoblasts, and its constitutive overexpression led to inhibition of osteoblast and adipocyte differentiation of human marrow stromal cells. Introduction: Molecular control of human mesenchymal stem cell (hMSC) differentiation into osteoblasts and adipocytes is not known. In this study, we examined the role of delta-like 1/preadipocyte factor-1 (Dlk1/Pref-1) in regulating the differentiation of hMSCs. Materials and Methods: As a model for hMSCs, we have stably transduced telomerase-immortalized hMSC (hMSC-TERT) with the full length of human Dlk1/Pref-1 cDNA and tested its effect on hMSC growth and differentiation into osteoblasts or adipocytes as assessed by cytochemical staining, FACS analysis, and real time PCR. Ex vivo calvaria organ cultures assay was used to confirm the in vitro effect of Dlk/Pref-1 on bone formation. Results: Dlk1/Pref-1 was found to be expressed in fetal and adult bone, hMSCs, and some osteoblastic cell lines. A retroviral vector containing the human Dlk1/Pref-1 cDNA was used to create a cell line (hMSC-dlk1) expressing high levels of Dlk1/Pref-1 protein. Overexpression of Dlk1/Pref-1 did not affect the proliferation rate of hMSC, but the ability to form mature adipocytes, mineralized matrix in vitro, and new bone formation in neonatal murine calvariae organ cultures was reduced. These effects were associated with inhibition of gene expression markers of late stages of adipocyte (adipocyte fatty acid-binding protein [aP2], peroxisome proliferator-activated receptor-gamma2 [PPAR,2], and adiponectin [APM1]) and osteoblast differentiation (alkaline phosphatase [ALP], collagen type I [Col1], and osteocalcin [OC]). Lineage commitment markers for adipocytes (adipocyte determination and differentiation factor ,1 [ADD1]) and osteoblasts (core binding factor/runt-related binding factor 2 [Cbfa1/Runx2]) were not affected. Conclusion: During hMSC differentiation, Dlk1/Pref-1 maintains the size of the bipotential progenitor cell pool by inhibiting the formation of mature osteoblasts and adipocytes. [source] Prostaglandin F2, inhibits adipocyte differentiation via a G,q-Calcium-Calcineurin-Dependent signaling pathwayJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2007Li Liu Abstract Prostaglandin F2, (PGF2,) is a potent physiological inhibitor of adipocyte differentiation, however the specific signaling pathways and molecular mechanisms involved in mediating its anti-adipogenic effects are not well understood. In the current study, we now provide evidence that PGF2, inhibits adipocyte differentiation via a signaling pathway that requires heterotrimeric G-protein G,q subunits, the elevation of the intracellular calcium concentration ([Ca2+]i), and the activation of the Ca2+/calmodulin-regulated serine/threonine phosphatase calcineurin. We show that while this pathway acts to inhibit an early step in the adipogenic cascade, it does not interfere with the initial mitotic clonal expansion phase of adipogenesis, nor does it affect either the expression, DNA binding activity or differentiation-induced phosphorylation of the early transcription factor C/EBP,. Instead, we find that PGF2, inhibits adipocyte differentiation via a calcineurin-dependent mechanism that acts to prevent the expression of the critical pro-adipogenic transcription factors PPAR, and C/EBP,. Furthermore, we demonstrate that the inhibitory effects of PGF2, on both the expression of PPAR, and C/EBP, and subsequent adipogenesis can be attenuated by treatment of preadipocytes with the histone deacetylase (HDAC) inhibitor trichostatin A. Taken together, these results indicate that PGF2, inhibits adipocyte differentiation via a G,q-Ca2+ -calcineurin-dependent signaling pathway that acts to block expression of PPAR, and C/EBP, by a mechanism that appears to involves an HDAC-sensitive step. J. Cell. Biochem. 100: 161,173, 2007. © 2006 Wiley-Liss, Inc. [source] PPAR,1 synthesis and adipogenesis in C3H10T1/2 cells depends on S-phase progression, but does not require mitotic clonal expansionJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2004Young C. Cho Abstract Adipogenesis is typically stimulated in mouse embryo fibroblast (MEF) lines by a standard hormonal combination of insulin (I), dexamethasone (D), and methylisobutylxanthine (M), administered with a fresh serum renewal. In C3H10T1/2 (10T1/2) cells, peroxisome proliferator-activated receptor ,1 (PPAR,1) expression, an early phase key adipogenic regulator, is optimal after 36 h of IDM stimulation. Although previous studies provide evidence that mitotic clonal expansion of 3T3-L1 cells is essential for adipogenesis, we show, here, that 10T1/2 cells do not require mitotic clonal expansion, but depend on cell cycle progression through S-phase to commit to adipocyte differentiation. Exclusion of two major mitogenic stimuli (DM without insulin and fresh serum renewal) from standard IDM protocol removed mitotic clonal expansion, but sustained equivalent PPAR,1 synthesis and lipogenesis. Different S-phase inhibitors (aphidicolin, hydroxyurea, l -mimosine, and roscovitin) each arrested cells in S-phase, under hormonal stimulation, and completely blocked PPAR,1 synthesis and lipogenesis. However, G2/M inhibitors effected G2/M accumulation of IDM stimulated cells and prevented mitosis, but fully sustained PPAR,1 synthesis and lipogenesis. DM stimulation with or without fresh serum renewal elevated DNA synthesis in a proportion of cells (measured by BrdU labeling) and accumulation of cell cycle progression in G2/M-phase without complete mitosis. By contrast, standard IDM treatments with fresh serum renewal caused elevated DNA synthesis and mitotic clonal expansion while achieved equivalent level of adipogenesis. At most, one-half of the 10T1/2 mixed cell population differentiated to mature adipocytes, even when clonally isolated. PPAR, was exclusively expressed in the cells that contained lipid droplets. IDM stimulated comparable PPAR,1 synthesis and lipogenesis in isolated cells at low cell density (LD) culture, but in about half of the cells and with sensitivity to G1/S, but not G2/M inhibitors. Importantly, growth arrest occurred in all differentiating cells, while continuous mitotic clonal expansion occurred in non-differentiating cells. Irrespective of confluence level, 10T1/2 cells differentiate after progression through S-phase, where adipogenic commitment induced by IDM stimulation is a prerequisite for PPAR, synthesis and subsequent adipocyte differentiation. © 2003 Wiley-Liss, Inc. [source] ErbB2 and EGFR are downmodulated during the differentiation of 3T3-L1 preadipocytes,,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2003Eleonora Pagano Abstract The expression of receptors belonging to the epidermal growth factor receptor subfamily has been largely studied these last years in epithelial cells mainly as involved in cell proliferation and malignant progression. Although much work has focused on the role of these growth factor receptors in the differentiation of a variety of tissues, there is little information in regards to normal stromal cells. We investigated erbB2 expression in the murine fibroblast cell line Swiss 3T3L1, which naturally or hormonally induced undergoes adipocyte differentiation. We found that the Swiss 3T3-L1 fibroblasts express erbB2, in addition to EGFR, and in a quantity comparable to or even greater than the breast cancer cell line T47D. Proliferating cells increased erbB2 and EGFR levels when reaching confluence up to 4- and 10-fold, respectively. This expression showed a significant decrease when growth-arrested cells were stimulated to differentiate with dexamethasone and isobutyl-methylxanthine. Differentiated cells presented a decreased expression of both erbB2 and EGFR regardless of whether the cells were hormonally or spontaneously differentiated. EGF stimulation of serum-starved cells increased erbB2 tyrosine phosphorylation and retarded erbB2 migration in SDS,PAGE, suggesting receptor association and activation. Heregulin-,1 and -,1, two EGF related factors, had no effect on erbB2 or EGFR phosphorylation. Although 3T3-L1 cells expressed heregulin, its specific receptors, erbB3 and erbB4, were not found. This is the first time in which erbB2 is reported to be expressed in an adipocytic cell line which does not depend on non EGF family growth factors (thyroid hormone, growth hormone, etc.) to accomplish adipose differentiation. Since erbB2 and EGFR expression were downmodulated as differentiation progressed it is conceivable that a mechanism of switching from a mitogenic to a differentiating signaling pathway may be involved, through regulation of the expression of these growth factor receptors. © 2003 Wiley-Liss, Inc. [source] CDK4 IVS4-nt40G,A and T2D-associated obesity in ItaliansJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2009Ramachandran Meenakshisundaram Cell cycle regulators play crucial roles in the preadipocyte proliferation and adipocyte differentiation. Cyclin-dependent kinase 4 (CDK4) mediates with D-type cyclins entry of cells into cell cycle in response to external stimuli. CDK4 plays a role in body weight, adipogenesis, and beta cell proliferation. CDK4 null mice develop type 2 diabetes (T2D). Furthermore, CDK4 variants are associated with obesity-associated tumors/cancer. We aimed at identifying a role of CDK4 IVS4-nt40G,,,A variant in T2D-associated obesity (body mass index, BMI,,,30) by association tests in an Italian T2D subjects dataset. We recruited from Italy 128 unrelated T2D subjects with BMI,<30,kg/m2 and 54 unrelated T2D subjects with BMI,,,30,kg/m2. We performed statistical power calculations in our dataset. DNA samples were directly sequenced with specific primers for CDK4 IVS4-nt40G,,,A variant. We identified a significant association of the G allele with T2D-associated obesity and of the A allele with T2D-associated BMI,<,30. In our study, we found that the CDK4 IVS4-nt40GG genotype is a risk variant for T2D-associated obesity and that the AA genotype is associated with BMI,<,30 in T2D. Hence, CDK4 IVS4-nt40A allele is protective and G allele confers risk for obesity in T2D patients. This study should prompt further work aiming at establishing CDK4 role in contributing to human obesity and T2D-associated obesity. J. Cell. Physiol. 221: 273,275, 2009. © 2009 Wiley-Liss, Inc. [source] Adipogenic Phenotype of Hepatic Stellate CellsALCOHOLISM, Issue 2005Hide Tsukamoto Abstract: Transdifferentiation of hepatic stellate cells (HSC) constitutes a major cellular event in the genesis of alcoholic liver fibrosis and cirrhosis and molecular mechanisms underlying this process is incompletely understood. Our laboratory proposed several years ago that HSC quiescence requires the transcriptional program known to be integral to preadipocyte to adipocyte differentiation. In support of the hypothesis, our research demonstrates the expression of adipogenic transcription factors (C/EBPs, PPAR,, SREBP-1c, LXR,) and adipocyte-specific genes (adipsin, resistin) are high in quiescent HSC and depleted in activated HSC. Three gain-of-function approaches have been taken to test this notion: the treatment of activated HSC with the adipocyte differentiation cocktail; ectopic expression of PPAR, or SREBP-1c. All three treatments coordinately upregulate a panel of putative adipogenic transcrition factors and cause morphologic and biochemical reversal of activated HSC to quiescent cells. These findings establish a new conceptual framework for the treatment of liver fibrosis and propose an intriguing notion concerning the plasticity of HSC. [source] In vitro interaction between mouse breast cancer cells and mouse mesenchymal stem cells during adipocyte differentiationJOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Issue 5 2009Feng Xu Abstract Surgical treatment following breast cancer, i.e. lumpectomy and mastectomy, may not efficiently remove all cancerous cells. As such, when mesenchymal stem cells (MSCs) are incorporated into the breast reconstruction process, it is likely that those MSCs will encounter remnant cancerous cells after transplantation into the defect site. The potential interaction between breast cancer cells and MSCs remains unclear. We hypothesized that paracrine interactions might occur between cells and various proteinases, growth factors and other cytokine molecules in the local microenvironment. Conditioned media (CM) from two mouse mammary cancer cell lines (4T1 and 4T07) and one mouse mammary epithelial cell line (NMuMG) were studied in the experimental model. Post-confluent mouse MSCs (D1 cells) were differentiated with an adipogenic hormonal cocktail. Conditioned media from the three cell types did not have an inhibitory effect on D1 cell viability; however, triglyceride (TG) and Oil red O (ORO) analysis results showed that 4T1-CM significantly inhibited D1 adipocyte differentiation and reduced lipid vesicle accumulation in the differentiating D1 cells. Preliminary analysis of the conditioned media revealed that a higher presence of matrix metalloprotease-9 (MMP-9) and urokinase plasminogen activator (uPA) was present in the 4T1-CM as compared to the levels found in 4T07-CM and NMuMG-CM, which were below the detection limit. Additionally, the conditioned medium of differentiated D1 cells on day 12 had a negative effect on 4T1 and 4T07 cell viability but no effect on NMuMG cell viability. The results suggest that mouse breast cancer cells modulate mouse MSC adipogenic differentiation, the level of modulation specific to the metastatic level. Copyright © 2009 John Wiley & Sons, Ltd. [source] Proteome analysis of adipocyte lipid rafts reveals that gC1qR plays essential roles in adipogenesis and insulin signal transductionPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 9 2009Ki-Bum Kim Abstract Since insulin receptors and their downstream signaling molecules are organized in lipid rafts, proteomic analysis of adipocyte lipid rafts may provide new insights into the function of lipid rafts in adipogenesis and insulin signaling. To search for proteins involved in adipocyte differentiation and insulin signaling, we analyzed detergent-resistant lipid raft proteins from 3T3-L1 preadipocytes and adipocytes by 2-DE. Eleven raft proteins were identified from adipocytes. One of the adipocyte-specific proteins was globular C1q receptor (gC1qR), an acidic 32,kDa protein known as the receptor for the globular domain of complement C1q. The targeting of gC1qR into lipid rafts was significantly increased during adipogenesis, as determined by immunoblotting and immunofluorescence. Since the silencing of gC1qR by small RNA interference abolished adipogenesis and blocked insulin-induced activation of insulin receptor, insulin receptor substrate-1 (IRS-1), Akt, and Erk1/2, we can conclude that gC1qR is an essential molecule involved in adipogenesis and insulin signaling. [source] Identification of target genes and pathways associated with chicken microRNA miR-143ANIMAL GENETICS, Issue 4 2010N. Trakooljul Summary MicroRNA (miRNA) is a family of small regulatory RNAs that post-transcriptionally regulate many biological functions including growth and development. Recently, the expression of chicken miRNA miR-143 was identified by using a deep sequencing approach. In other vertebrate species, miR-143 functions as a regulator of adipocyte differentiation and as a tumour suppressor. However, little is known about the biological function(s) of miR-143 in chickens. To study the functions of chicken miR-143, DNA microarray analysis and a dual luciferase reporter assay were employed to identify genes directly targeted by miR-143 as well as other biologically relevant genes. Microarray analysis indicated that 124 genes were differentially expressed upon in vitro anti- miR-143 treatment in embryonic chick splenocytes (P -value cutoff <0.01). Many of these genes are associated with cell proliferation, apoptosis and tumourigenesis. Six of the up-regulated genes possess at least one potential miR-143 binding site in their 3,UTRs, of these the binding sites of PYCR2, PSTPIP1 and PDCD5 were validated by an in vitro luciferase reporter assay. In addition, several potential targets with important biological functions were identified by the miRanda algorithm and experimentally confirmed. These targets include KLF5, MAP3K7, TARDBP and UBE2E3, which have conserved miR-143 binding sites across multiple vertebrate species. Potential chicken specific miR-143 target sites were also validated for LPIN1, PCK2, PYCR2, METTL14, SLC2A2 and TNFSF10. Overall, the current study suggests that miR-143 is ubiquitously expressed among tissues and is likely to be involved in the regulation of cell proliferation and apoptosis. [source] Differentially expressed genes during bovine intramuscular adipocyte differentiation profiled by serial analysis of gene expressionANIMAL GENETICS, Issue 4 2010Y. Mizoguchi Summary Beef marbling or intramuscular fat deposition is an economically important carcass trait in Japanese Black cattle. To investigate genes involved in intramuscular adipogenesis, differential gene expression during adipogenesis in a clonal bovine intramuscular preadipocyte (BIP) cell line was profiled with serial analysis of gene expression (SAGE). We sequenced 75 283 tags for the proliferation phase (day 0) and 81 878 tags for the differentiation phase (4 days after adipogenic stimulation: day 4). A comparison of the unique SAGE tag frequencies between the day 0- and day 4-libraries revealed that 878 (2.8%) of the 30 989 unique putative transcripts were expressed at significantly different levels (P < 0.05); 401 tags (1.4%) were up-regulated and 477 tags (1.2%) were down-regulated in the day 4-library relative to the day 0-library. We confirmed up-regulation of 10 tags of the genes that were up-regulated in the previous subtraction cloning studies in BIP cells [Animal Science Journal, 76 (2005) 479]. Of the 878 differentially expressed tags, 377 were identified in the bovine RefSeq library and 356 were assigned a bovine draft genomic sequence. Fifteen tags were mapped in previously detected beef marbling quantitative trait loci (QTL) regions [Mammalian Genome, 18 (2007) 125]. These genes may be involved in the adipogenic processes of beef marbling. [source] Expression of DLK1 splice variants during porcine adipocyte development in vitro and in vivoANIMAL GENETICS, Issue 2 2009J. Samulin Summary Delta-like 1 (DLK1) belongs to the epidermal growth factor-like transmembrane protein family and is involved in the regulation of adipogenesis. Several splice variants of DLK1 have been identified in various species, of which two have been previously identified in pig. Here, we present two novel porcine DLK1 splice variants DLK1A and DLK1C. The gene expression profile of these variants together with the previously described DLK1B and DLK1C2 variants was studied in adipose tissue depots of pigs and during adipocyte differentiation in vitro. The short DLK1C and DLK1C2 transcripts were most abundantly expressed and their expression was reduced during porcine adipogenesis. [source] Changes in peroxisome proliferator-activated receptor gamma gene expression of chicken abdominal adipose tissue with different age, sex and genotypeANIMAL SCIENCE JOURNAL, Issue 3 2009Kan SATO ABSTRACT Peroxisome proliferatior-activated receptor gamma (PPAR,) is a transcription factor that regulates adipocyte differentiation, and the activation of PPAR, increases fat deposition in growing chickens. The aim of the present study was to investigate whether the levels of PPAR, gene expression were related to fat pad weight in abdominal adipose tissue in growing chickens with different genotype and sex. Body weight and abdominal adipose tissue weight in broiler chickens (Ross strain) were higher than the other genotypes (Road Island Red, White Leghorn, and Japanese native poultry (Tsushima)) at 3 and 5 weeks of age. PPAR, mRNA expression in abdominal adipose tissue tended to increase with age, as evidenced by higher expression levels at 5 weeks than at 1 week of age in all sex and genotype of chickens. In broiler chickens, the PPAR, expressions were significantly higher than the other genotypes. PPAR, mRNA expression levels in abdominal adipose tissue of female chickens rapidly increased at 3 weeks, and were unchanged until 5 weeks, while those in male chickens gradually increased until 5 weeks. In addition, abdominal adipose tissue weight was correlated with PPAR, expression levels. These results demonstrated that PPAR, gene expression is a useful marker of fat deposition in chickens, suggesting that PPAR, is a key factor of fat accumulation in chicken abdominal fat pad. [source] Glucocorticoid-induced differentiation of primary cultured bone marrow mesenchymal cells into adipocytes is antagonized by exogenous Runx2APMIS, Issue 8 2010LE LIN Lin L, Dai S-Dong, Fan G-Yu. Glucocorticoid-induced differentiation of primary cultured bone marrow mesenchymal cells into adipocytes is antagonized by exogenous Runx2. APMIS 2010; 118: 595,605. Long-term clinical use of glucocorticoids often causes the serious side effect of non-traumatic avascular osteonecrosis. The aim of this study was to examine the effects and mechanisms of a glucocorticoid, dexamethasone (Dex), on differentiation of primary cultured rat bone marrow mesenchymal cells (BMCs). We also tried to block the inhibitory effects of Dex on osteoblast differentiation. Adipocyte markers (peroxisome proliferator-activated receptor,-2 and aP2) were increased in response to Dex treatment in a dose- and time-dependent manner, while osteoblastic markers [Runx2, COL 1, osterix, alkaline phosphatase (ALP) and OC] were down-regulated, consistent with ALP and osteocalcin promoter activity. To validate the effects of Runx2 on the expression of osteogenesis and adipocyte genes, pCMV/Flag-Runx2 was transfected into BMCs, and relevant markers were detected after 10,7 M Dex treatment for 48 h. The results indicated that Dex treatment induced adipogenic differentiation and suppressed proliferation. No significant difference was detected in expressions of these genes between Runx2-transfected cells and Dex-treated BMCs. These data suggest that Dex primarily induced adipocyte differentiation of BMCs. Exogenous Runx2 can antagonize the effect of Dex on osteoblast differentiation. [source] Altered expression of CCAAT/enhancer binding protein and FABP11 genes during adipogenesis in vitro in Atlantic salmon (Salmo salar)AQUACULTURE NUTRITION, Issue 1 2010T.-S. HUANG Abstract The study of CCAAT/enhancer binding proteins (C/EBPs) is important in the understanding of adipogenesis, but little is known about their regulation in fish. Here, we report three Atlantic salmon orthologs of c/ebp, and their expression in different tissues and in adipogenesis in vitro. During differentiation the expression of c/ebp, and fatp1 were upregulated in early differentiation stage with continuing high expression level in mature adipocytes, whereas c/ebp, and fabp11 expression were elevated in mature adipocytes. Furthermore, the fatty acids eicosapentaenoic (EPA) and docosahexaenoic (DHA), suppressed the expression of the c/ebps, ppar,, and fatty acid transport protein (fatp1) during terminal adipocyte differentiation. The study indicates that C/EBPs are induced upon the differentiation of primary-cultured adipocytes from Atlantic salmon and that marine n-3 highly unsaturated fatty acids (HUFAs) affect the c/ebps expressions in mature adipocytes. Therefore, the established cell model described here appears to be valuable for studying modulation of fat content in farmed Atlantic salmon. [source] Carotenoids and retinoids as suppressors on adipocyte differentiation via nuclear receptorsBIOFACTORS, Issue 1-4 2000Teruo Kawada Abstract The adipocyte differentiation program is regulated by the sequential expression of transcriptional activators, mainly peroxisome proliferator activated receptor (PPAR) families. In the present study, we have decided to systematically examine the effects of vitamin A and its precursors, carotenoids and retinoids, on terminal differentiation from preadipocytes to adipocytes on the cellular and molecular aspects. The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators. RAR,, RAR,, RXR,, and RXR, mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. The autoregulated amplification of RAR, mRNA was observed by these own ligands in 3T3-L1 cells. And, RA inhibited PPAR,2 expression more effectively and caused concomitantly a greater inhibition of adipocyte differentiation. These results suggest that the inhibitory action of adipocyte differentiation by carotenoids and retinoids are exhibited through the RAR up-regulation and the suppression of PPAR,2. The nature of the cross talk of vitamin A actions between the RARs, RXRs and PPARs via co-activator in adipose tissue will likely prove to be important for understanding the process of adipogenesis. [source] | ||||||||||||||||