Publication for Cd36 and Pparg

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Cd36 CD36 molecule 12491 [link]
mmu Pparg peroxisome proliferator activated receptor gamma 19016

Pubmed ID Priority Text
26050669 0.99 PPARgamma more efficiently binds to PRDM16 (see pr domain-containing protein-16), a powerful transcriptional coactivator of brown fat genes (Fig. 1).
0.99 fat-specific genes and facilitates the binding of other transcription factors, including PPARgamma (Fig. 2).
0.98 fat cell differentiation is coordinated by peroxisome proliferator-activated receptor (PPAR)-gamma and members of the c/EBP family of transcription factors.
0.98 PPARgamma, in collaboration with c/EBPalpha, binds and regulates the expression of most adipocyte-related genes in fat cells.
0.98 fat programming of adipocytes, PPARgamma is intimately involved in regulating brown adipocyte-selective characteristics of adipocytes.
0.98 PPARgamma participates in the activation of brown fat genes, including Ucp1.
0.98 PPARgamma binds to many brown (vs. white) fat-specific genes in brown fat cells and tissue.
0.98 PPARgamma activators, especially those in the thiazolidinedione (TZD) class, are particularly potent activators of mitochondrial biogenesis and brown fat-selective genes in adipocytes, including Ucp1.
0.98 fat genes involves the activation of SIRT1, an NAD-dependent deacetylase that deacetylates two residues in PPARgamma.
0.98 fat-selective genes, including Ucp1 (using the same element as PPARgamma in the -2.5-kb enhancer), Prdm16, and Pgc1alpha, which are key drivers of brown fat differentiation.
0.98 PPARgamma bind together and activate brown fat-selective target genes in rosi-treated adipocytes.
0.98 PPARgamma, which leads to enhanced activation of white fat genes.
0.98 PPARgamma is a master regulator of white and brown/beige fat differentiation, but how PPARgamma (and for that matter, PRDM16) is recruited to brown genes in BAT has been unclear.
0.98 fat-specific binding sites of PPARgamma (and PRDM16-binding sites in BAT) were found to be highly enriched with a DNA motif for early B-cell factor (EBF).
0.97 PPARgamma to stimulate the transcription of brown fat genes.
0.95 PPARgamma agonists regulate the development of beige or brown fat cells in vivo remains an important question.
0.94 PPARgamma to PRDM16 and cooperates with PPARgamma to activate a white fat gene profile.
21949655 0.98 CD36 downregulation in inflammatory conditions is associated with a failure in the expression and activation of PPARgamma.
0.98 PPARgamma-deficient macrophages, we establish that in inflammatory conditions, the Nrf2 transcription factor controls CD36 expression independently of PPARgamma.
0.98 PPARgamma ligands, enhance CD36 expression and CD36-mediated Plasmodium phagocytosis.
0.98 CD36 expression through PPARgamma nuclear receptor is inefficient under malaria inflammatory processes.
0.98 PPARgamma to promote CD36 expression and its associated functions in inflammatory conditions.
0.98 CD36 expression is under the transcriptional control of a PPARgamma nuclear receptor.
0.98 PPARgamma ligands, such as thiazolidinediones, or IL4 and IL13 Th2 cytokines, promote CD36 expression on macrophages.
0.98 CD36 downregulation was correlated with a marked reduction in PPARgamma activation upon TNF-alpha stimulation.
0.98 PPARgamma to promote CD36 expression and hence CD36-mediated phagocytosis of PfPEs during acute inflammatory processes.
0.98 CD36 expression in inflammatory conditions independently of PPARgamma both on murine and human inflammatory macrophages.
0.98 CD36 expression and CD36-mediated PfPEs phagocytosis through downregulation of PPARgamma.
0.98 CD36 expression and reveals the failure of PPARgamma ligands to promote CD36 expression on macrophages in these conditions.
0.98 PPARgamma activators to promote CD36 expression and its PfPEs phagocytosis-associated function in inflammatory conditions strongly suggests that PPARgamma is no longer able to exert its transcriptional activity on the CD36 promoter.
0.98 PPARgamma ligands to enhance CD36 expression and its antimalarial associated functions in inflammatory conditions was associated with a marked decrease of PPARgamma expression.
0.98 CD36 protein level after the administration of Nrf2 or PPARgamma activators before the onset of inflammation demonstrate that both Nrf2 and PPARgamma ligands prevent the downregulation of CD36 expression.
0.98 PPARgamma, Nrf2 activators are able to promote CD36 expression.
0.98 CD36 expression independently of PPARgamma.
0.98 CD36 expression on hMDMS via the PPARgamma signaling pathway was associated with a marked reduction of PPARgamma mRNA and protein levels (Fig. 6B) during acute inflammatory processes.
0.98 CD36 protein level on macrophages only increased after in vivo SFN treatment (Fig. 7F), demonstrating that in an in vivo acute inflammatory context only Nrf2 activators and not PPARgamma ligands are able to up-regulate CD36 expression.
0.98 PPARgamma ligand can in vitro and in vivo improves the outcome of experimental malaria in mice, enhancing CD36-mediated PEs phagocytic processes and limiting parasite-induced inflammatory processes.
0.98 PPARgamma ligands thiazolidinediones and IL4 or IL13, two Th2 cytokines known to activate PPARgamma, were previously shown in vitro to promote CD36 expression and enhance CD36-mediated PEs phagocytosis.
0.98 PPARgamma in swiss murine macrophages and human monocyte-derived macrophages, resulting in a failure to trigger this pathway to promote CD36 expression and Plasmodium clearance.
0.98 PPARgamma and CD36 in hMDMS, and monocytes from Plasmodium-infected patients exhibit a CD36 dowregulation.
0.98 PPARgamma-/- macrophages did not present a totally abolished CD36 phenotype, suggesting the existence of alternative pathways controlling CD36 expression on macrophages.
0.98 PPARgamma to promote CD36 expression during acute inflammatory processes.
0.98 CD36 expression in absence or in the presence of PPARgamma nuclear receptor.
0.98 CD36 expression and improves the outcome of severe malaria independently of PPARgamma.
0.97 PPARgamma ligands were unable to promote CD36 expression and subsequently to restore the loss of CD36-mediated Plasmodium clearance.
0.97 CD36 expression, could substitute the deficiency of PPARgamma in acute inflammatory conditions to enhance the expression of the CD36 receptor.
0.97 PPARgamma and Nrf2 activators has been observed in vitro on macrophage CD36 expression in inflammatory conditions (Fig. S2D).
0.97 CD36 over-expression following rosiglitazone or IL13 treatments failed in PPARgamma deficient macrophages (PPARgamma-/-), while SFN or DEM treatments enhanced CD36 expression in PPARgamma-/- cells (Fig. 3D).
0.97 CD36 expression and CD36 mediated-P. falciparum phagocytosis in absence of PPARgamma.
0.97 PPARgamma and hence CD36 expression in C57BL/6 murine macrophages, suggesting the importance of genetic background in their regulation.
0.97 CD36 receptor following an anti-TNF-alpha antibody treatment occurred independently of PPARgamma and involved radical oxygen species production (ROS) via NADPH oxidase activation.
0.97 CD36 induction following SFN or DEM treatments was shown to be PPARgamma independent and Nrf2 dependent.
0.97 CD36-mediated parasite clearance due to a downregulation of PPARgamma.
0.95 CD36 expression via an activation of the nuclear receptor PPARgamma, could reverse the downregulation of CD36 receptor induced by inflammatory conditions.
0.95 PPARgamma ligands and IL13 have no effect on the modulation of CD36 expression in inflammatory macrophages.
0.94 CD36 by Nrf2 activators is independent of PPARgamma.
0.91 CD36 was promoted by rosiglitazone, IL13, SFN or DEM treatments in macrophages from PPARgamma+/+ mice.
0.91 PPARgamma and CD36 on macrophages from C57BL/6 mice in inflammatory conditions while PPARgamma and CD36 were greatly impaired in swiss macrophages, as in hMDMs.
0.89 PPARgamma Alternative Pathway to Promote CD36 Expression on Inflammatory Macrophages: Implication for Malaria
0.87 CD36-dependent PPARgamma transcriptional activity was correlated with a lower level of PPARgamma expression, we evaluated PPARgamma protein and mRNA levels in an inflammatory context.
0.80 PPARgamma specific activators, IL13 and rosiglitazone, did not change the CD36 protein level, whereas the Nrf2 activators (SFN or DEM) strongly enhanced CD36 protein expression (Fig. 3B).
0.78 CD36 expression in absence of PPARgamma, we studied CD36 mRNA expression in macrophages in which PPARgamma had been selectively disrupted.
0.68 CD36 expression in absence of the PPARgamma nuclear receptor, we performed experiments on the RAW 264.7 macrophage murine cell line which expresses a very low level of PPARgamma, as demonstrated in Fig. 3A.
29383825 0.98 PPARgamma specifically in inguinal fat tissue in aging mice is associated with increased fat tissue expansion and insulin resistance.
0.98 PPARgamma downregulation in young and mid-aged mice demonstrate a preferential regulation of brown fat gene programs in inguinal fat in an age-dependent manner.
0.98 PPARgamma, one of the members of this subfamily, is required for the development of all types of fat cells and functions as a regulator of both white and brown gene programs in adipocytes (Lefterova, Haakonsson, Lazar & Mandrup, 2014; Tontonoz & Spiegelman, 2008).
0.98 PPARgamma has also been shown to directly bind to PPAR response element in promoters of brown fat-selective genes, such as UCP1, Cidea, and Elovl3, and to induce them transcriptionally (Sears, MacGinnitie, Kovacs & Graves, 1996; Viswakarma et al., 2007; Kobayashi & Fujimori, 2012).
0.98 PPARgamma ablation in subcutaneous fat tissue of young and old mice revealed PPARgamma preferential regulation of brown fat gene programs depending on the age of the mice.
0.98 PPARgamma knockdown in iWAT of young mice is associated with decreased fat amount and reduced adipocyte size (Figure 5c-e), consistent with the lipodystrophic phenotype previously reported in fat-specific PPARgamma knockout mice (He et al., 2003; Jones et al., 2005; Wang et al., 2013).
0.98 PPARgamma selectively in iWAT in aging mice led to an increase in both the amount of subcutaneous fat and in the size of its adipocytes (Figure 5c-e).
0.98 PPARgamma knockdown have a selective reduction in the expression of white fat gene targets such as Agt, Retn/Resistin, Slc2a4/Glut4, Cfd/Adiposin, Adipoq/Adiponectin, and Fabp4/aP2 (Figure 6a,b), while downregulation of PPARgamma in aging mice affects specifically brown fat genes such as Dio2, Pparalpha, Prdm16, and Ucp1 (Figure 6a,c).
0.97 PPARgamma in fibroblasts in vitro has been shown to drive adipogenesis (Mueller et al., 2002; Tontonoz, Hu & Spiegelman, 1994), and its selective ablation in fat leads to reduced adipose tissue mass and lipodystrophy (He et al., 2003; Jones et al., 2005; Wang, Mullican, DiSpirito, Peed & Lazar, 2013).
0.97 PPARgamma-loxP mice (PPARgamma-iWAT-KO) or shPPARgamma adenovirus in C57 mice (PPARgamma-iWAT-KD) led to modulation of PPARgamma levels in subcutaneous fat tissue.
0.97 PPARgamma is required for the maintenance of brown fat programs in iWAT of aging mice.
0.97 PPARgamma preferentially regulates brown gene programs in inguinal fat of aging mice.
0.96 PPARgamma ablation in every fat tissue generated by crossing PPARgamma-LoxP mice with either aP2- or adiponectin-Cre mice revealed impaired fat development and reduced fat mass (He et al., 2003; Jones et al., 2005; Wang et al., 2013).
0.96 fat gene programs, with no changes in white gene programs (Figure 4d), and immunohistochemistry of iWAT revealed decreased UCP1 staining in mice with PPARgamma deficiency (Figure 4e).
0.95 PPARgamma targets common to both white and brown fat tissues, as well as depot-selective ones (Siersbaek et al., 2012).
0.95 PPARgamma occurring specifically in aging could modify PPARgamma target gene promoter binding choices by potentially altering PPARgamma affinity for specific cofactors, given that it has been previously demonstrated that the recruitment of brown fat coactivators can be modulated by the PPARgamma acetylation status in young mice (Qiang et al., 2012) and that phosphorylation of PPARgamma promotes the interaction with specific coregulators (Choi et al., 2014).
0.94 PPARgamma deficiency in iWAT may differentially affect white and brown fat gene programs depending on the age of the mice.
0.94 PPARgamma ablation on fat tissue reported in published aP2- and adiponectin-driven knockout models and in our study of young mice may be due to the differences in the spatiotemporal conditions of PPARgamma ablation, given that PPARgamma deletion was previously achieved in every fat depot during development and in adult mice (He et al., 2003; Jones et al., 2005; Wang et al., 2013), while here PPARgamma levels are selectively reduced in subcutaneous fat tissue in mid-aged mice.
0.94 PPARgamma to brown fat gene promoters we observed in 12-month-old mice is driven by differential amounts of brown versus white cofactors present in subcutaneous adipose tissues in aging mice.
0.93 PPARgamma mRNA levels in epididymal WAT and BAT depots nor in tissues such as liver and pancreas (Figure 1d), suggesting the PPARgamma deficiency was indeed achieved selectively in subcutaneous fat tissue.
0.92 PPARgamma selectively in subcutaneous fat during late stages of life, it remains to be determined whether PPARgamma can specifically affect browning of subcutaneous tissue during the aging process.
0.92 PPARgamma-iWAT-KO and PPARgamma-iWAT-KD mice showed increased total body weight (Figure 2a), and nuclear magnetic resonance (NMR) scan assessment of body composition revealed a selective increase in fat mass while no changes in lean mass were observed (Figure 2b,c).
0.92 PPARgamma deficiency selectively in subcutaneous fat during aging is associated with increased adiposity are surprising given that they are sharply in contrast with the lipodystrophic phenotype and the impairment in adipose tissue expansion previously reported in aP2- and adiponectin-driven fat-specific PPARgamma KO mice (He et al., 2003; Jones et al., 2005; Wang et al., 2013) and in young mice with decreased PPARgamma levels selectively in iWAT (Figure 5).
0.90 PPARgamma in fat depots, liver, pancreas, and macrophages present in iWAT.
0.90 PPARgamma in fat tissue biology, in this study we sought to determine the role of PPARgamma in aging-associated metabolic decline.
0.89 PPARgamma controls gene programs in an age- and depot-dependent manner, we downregulated PPARgamma levels in iWAT of young and aging mice via unilateral injections in subcutaneous fat of control or shPPARgamma adenoviruses (Figure 5a,b).
0.89 PPARgamma at the promoters of aP2 and Ucp1 occurring in aging, given that those genes represent markers of white and brown fat programs, respectively.
0.88 PPARgamma in subcutaneous fat exacerbates age-associated obesity and metabolic decline
0.88 PPARgamma in inguinal adipose tissue via injections of adenoviruses expressing Cre or shPPARgamma directly into iWAT of PPARgamma-LoxP or C57BL/6J aging mice, respectively, to assess the selective role of PPARgamma in subcutaneous fat tissue at late life stages.
0.87 fat gene expression in mice with PPARgamma deficiency in iWAT
0.75 fat cells interspersed in inguinal fat tissue expend energy via creatine metabolism (Kazak et al., 2015), it is of interest to assess whether the effects of PPARgamma reported here involve alternative futile cycles in addition to classical thermogenic pathways.
0.74 fat depot and life stage in which one of the two opposed PPARgamma functions, adipogenic and thermogenic, is predominant.
0.54 PPARgamma selectively in subcutaneous fat tissue of mid-aged mice via adenoviral injections
30186237 0.98 PPARgamma agonists, PRDM16 induces multiple PPARgamma target genes in adipogenesis like aP2 and adiponectin, as well as brown fat-selective gene program, including Ucp1 and Cidea.
0.98 PPARgamma agonists could induce a white-to-brown fat conversion through stabilization of PRDM16 protein, suggesting the existence of a positive regulatory loop to strengthen the interaction of the PPARgamma/PRDM16 complex to maintain the thermogenic capacity in beige adipocytes.
0.98 PPARgamma/PRDM16 complex and facilitate its function in brown/beige fat identity determination.
0.98 PPARgamma recruits EBF2 to its brown-selective binding site and coactivates the expression of brown fat-selective genes such as Ucp1, Pparalpha, and Prdm16.
0.98 fat identify via inhibition of EBF2 and PRDM16 activity, further suggesting the critical role of PPARgamma/PRDM16/EBF2 in brown adipocyte development.
0.98 fat, the PPARgamma/PRDM16 complex recruits another distinct set of cofactors to promote brown/beige fat function in adaptive thermogenesis and energy homeostasis, among which PPARgamma-coactivator PGC1alpha plays a central role.
0.98 fat, PGC1alpha promotes mitochondrial biogenesis and thermogenesis at least partially by coactivating PPARgamma and enhancing PPARgamma's transcription activity on the thermogenic gene program, including Cidea, Elovl3, and Ucp1.
0.98 PPARgamma/PRDM16 complex also impacts the induction of brown fat gene programs and thus the brown/beige fat function.
0.98 PPARgamma Lys268 and Lys293 facilitate the close interaction between PPARgamma and PRDM16 and is essential for the selective induction of brown fat-selective genes and repression of visceral white fat-selective genes.
0.98 PPARgamma at the brown fat specific enhancers and facilitate PPARgamma chromatin accessibility for induction of brown fat gene programs through mechanisms independent of the PPARgamma/PRDM16 complex.
0.98 PPARgamma preferentially binds to the promoters of browning vs. whitening gene program, thus maintains browning capability of subcutaneous fat of aging mice rather than lipid storage, as shown by gene program expression array and in vivo ChIP analysis (Figure 1).
0.98 PPARgamma expression levels are dramatically induced by CR treatment in metabolic organs, especially in inguinal fat for browning of white fat, suggesting that PPARgamma activation might mimic CR effects at least in fat tissues.
0.97 PPARgamma2 expresses the highest in adipose tissues and is highly inducible in other tissues under high fat diet (HFD).
0.97 PPARgamma in adipose tissues consistently lead to impaired adipocyte differentiation and reduced fat weights or lipodystrophy, though different animal models show improved or worsen insulin sensitivity depend on the extent of PPARgamma deficiency.
0.97 PPARgamma/PRDM16 complex on the promoters of brown fat-selective genes.
0.97 PPARgamma function in the brown fat and are prone to obesity due to reduced energy expenditure and fatty acid oxidation upon HFD feeding.
0.97 fat, PPARgamma preferentially recruits SRC-2 as its coactivator to transactivate downstream fat uptake and storage pathways while in the brown fat SRC-2 competes with SRC-1 for PPARgamma binding and disrupts SRC-1-induced interaction between PPARgamma and PGC1alpha.
0.97 PPARgamma/PRDM16/PGC1alpha thermogenic transcriptional complex ensures delicate regulation on brown/beige fat functions by fine tuning its various components and modification status.
0.97 PPARgamma and its cofactors in fat biology during development or in young adult animals have been extensively studied.
0.97 PPARgamma specifically in subcutaneous fat in aging mice (12-month-old) is sufficient to increase body weight and insulin resistance by accelerating the decay of browning effects of white fat and disrupting energy homeostasis.
0.97 PPARgamma in adipose tissues during various stages of the adipocyte life cycle and the resulting regulatory function on fat development, thermogenesis and adipocyte senescence (Figure 2).
0.96 PPARgamma2 level, resulting in body weight reduction, fat mass decrease and fat redistribution in knockout mice.
0.96 PPARgamma deletion in a temporal-specific manner in inguinal fat of aging animals causes significant increases in body weight and fat mass, which is in sharp contrast to young control animals.
0.95 PPARgamma activation via its full agonists, thiazolidinediones, has been shown to improve insulin sensitivity and induce browning of white fat, while undesirably induce weight gain, visceral obesity and other adverse effects.
0.95 PPARgamma on the genome-wide scale in white, brown and beige adipocytes under different metabolic conditions, which enable us to gain a deeper understanding of the common and distinct target gene sets regulated by PPARgamma in different fat depots, under different diet regimes or ages, or in response to different environmental or drug stimulus.
0.93 PPARgamma downstream brown fat-selective gene program, EBF2 deficient mice fail to thrive due to severe defects in brown fat development and themogenesis.
0.89 PPARgamma in beige fat during aging.
0.65 fat cell cDNA library through yeast two-hybrid system using PPARgamma partial protein as bait.
0.56 PPARgamma-centered complex in the regulation of Adipogenesis (A), Brown/beige fat identity (B), Brown/beige fat function (C), Brown/beige fat senescence (D) and Diabetic gene program (E).
21704731 0.98 PPARgamma activity is increased in subcutaneous compared to visceral fat tissues, which may account for the high expression of PPARgamma target genes that define properties of subcutaneous fat.
0.98 PPARgamma, C/EBPalpha is also preferentially expressed in subcutaneous compared to visceral fat, where it is likely to contribute to the increase in PPARgamma activation in this tissue (Figure 1, Group 2).
0.98 PPARgamma expression and adipogenesis in NIH-3T3 cells, but the role of this pathway in fat formation in vivo has not been elucidated yet.
0.98 PPARgamma raises questions about mechanisms controlling the expression of this transcription factor and the contribution of this pathway to PPARgamma induction in fat depots.
0.98 fat in Aldh1a1-/- versus WT female mice, PPARgamma expression was markedly diminished in visceral compared to subcutaneous fat (70% vs 40%) (Figure 3).
0.98 PPARgamma and fat formation (Figure 3).
0.98 fat formation and PPARgamma expression
0.98 fat, which in turn induces PPARgamma expression.
0.97 PPARgamma in a fat-depot-specific manner, and suggest the important contribution of this autocrine pathway in the development of visceral obesity.
0.97 PPARgamma-mediated activation of adiponectin has already been recognized as a major mechanism for insulin sensitivity associated with subcutaneous fat.
0.97 fat distribution also proceeds through PPARgamma regulation, although PPARgamma involvement could be somewhat paradoxical in the context of autocrine mechanisms for glucocorticoid production.
0.97 fat diet-induced obesity, but accompanied by increased expression of PPARgamma in mouse fat.
0.97 PPARgamma expression was similar (data not shown), but expression of PPARgamma target genes was reduced in Aldh1a1-/- compared to WT mice on a high-fat diet.
0.97 fat diet in adipose tissue development and PPARgamma expression, whereas treatment of obese mice on a regular diet with vitamin A resulted in decreased fat mass ( and reviewed in this issue).
0.97 fat expresses higher levels of PPARgamma, C/EBPalpha, and CREBP1 compared to visceral fat
0.96 PPARgamma2 performance in patients with PPARgamma2 Pro12Ala (P12A) polymorphism leads to overweight, prevailing loss of subcutaneous fat, insulin resistance, and other metabolic dysfunctions in children and lean adults.
0.96 PPARgamma expression in visceral fat and a 40% decrease in PPARgamma expression in subcutaneous fat, as compared to WT, which corresponds to fat accumulation in visceral and subcutaneous depots.
0.95 PPARgamma expression can contribute causally to the formation of specific fat depots.
0.93 PPARgamma and C/EBPalpha in these mice as compared to WT mice, and deficient fat formation, although these differences were not seen in adult mice.
0.84 fat in adult mice with pRb deficiency in adipose tissue was not associated with alteration of PPARgamma expression.
29491646 0.98 CD36 and the peroxisome proliferator-activated receptor gamma (PPAR-gamma).
0.98 CD36 and PPAR-gamma in oxLDL-stimulated RAW264.7 cells and ApoE-/-mice, in the latter case by regulating heme oxygenase-1.
0.98 CD36 is mediated by the activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma) which is involved in energy balance and the regulation of adipocyte differentiation.
0.98 CD36 as well as the downstream transcription factor PPAR-gamma.
0.97 CD36-and PPAR-gamma-mediated differentiation of macrophages.
0.97 CD36 and PPAR-gamma in oxLDL-stimulated macrophages mediate the development of atherosclerotic lesions.
0.97 CD36 and PPAR-gamma, whereas DSE significantly reduced this response, up to a maximum at 2 mg/mL [Figure 1a and b].
0.97 CD36 and PPAR-gamma in oxLDL-stimulated RAW264.7 cells and in the aorta of ApoE-/-mice.
0.97 CD36, and PPAR-gamma, and it inhibits the differentiation of macrophages into foam cells.
0.96 CD36 and peroxisome proliferator-activated receptor gamma in oxidative low-density lipoprotein-stimulated RAW264.7 Cells and ApoE Knockout (ApoE Knockout [ApoE-/-]) mice
0.96 CD36 and peroxisome proliferator-activated receptor gamma in oxidative low-density lipoprotein-stimulated RAW264.7 Cells.
0.96 CD36 and PPAR-gamma in AE mice.
0.95 CD36 and peroxisome proliferator-activated receptor gamma in ApoE knockout mice.
0.94 CD36 and peroxisome proliferator-activated receptor gamma in oxidative low-density lipoprotein-stimulated RAW264.7 cells
0.94 CD36 and PPAR-gamma expression.
0.93 CD36 and PPAR-gamma expression in vitro and in vivo.
0.92 CD36 and PPAR-gamma were also significantly higher in the aorta of AE group mice than control mice.
0.87 CD36 and PPAR-gamma activity may be a suitable therapeutic approach for atherosclerosis.
0.85 CD36 and peroxisome proliferator-activated receptor gamma in ApoE knockout mice
0.80 CD36 and PPAR-gamma (to 50.4% and 71% for CD36 and PPAR-gamma, respectively).
32256662 0.98 PPARgamma in visceral fat and skeletal muscle and the expression of LPL in skeletal muscle.
0.98 Peroxisome proliferator-activated receptor gamma (PPARgamma) is located in the p25 region of chromosome 3 and is a class of ligand-activated nuclear transcription factors that play a key role in lipid metabolism, fat cell formation, and various biological processes like inflammation.
0.98 PPARgamma can regulate the expression of lipoclastic differentiation related factors such as LPL and promote lipid oxidation, thereby regulating the fatty acid metabolism in fat and muscle tissues.
0.97 PPARgamma activation can reduce fatty acids transported to the liver and muscle and reduce fat synthesis, which inhibits lipid metabolism.
0.97 PPARgamma mRNA in visceral fat was downregulated in the HFD group, whose mice were provided a high-fat diet (P < 0.05).
0.94 PPARgamma and LPL were detected in the skeletal muscle tissue and visceral fat to explore the possible molecular mechanism that ECD plays in eliminating phlegm.
0.94 PPARgamma is widely distributed in fat, skeletal muscle, heart muscle, and liver tissues.
0.94 fat expression in LPL and PPARgamma illustrates the effectiveness of ECD in eliminating phlegm.
0.93 PPARgamma mRNA and protein level in visceral fat and PPARgamma and LPL protein level in skeletal muscle in the ECD group.
0.92 fat diet by affecting PPARgamma and LPL.
0.87 PPARgamma mRNA and protein in the visceral fat of mice was higher than that in the HFD group (P < 0.05), and the expression of LPL mRNA and protein was lower than that in the HFD group (P > 0.05).
0.85 PPARgamma can be expressed in fat, kidney, spleen, and skeletal muscle, although most current studies concentrate on fat and skeletal muscle.
0.85 fat tissue, it could increase the activity of PPARgamma in the visceral fat, inhibit the action of LPL to accelerate fat deposition in visceral fat, and improve the IR in the adipose tissue.
0.81 PPARgamma and LPL, the expression levels of PPARgamma, LPL mRNA, and protein in visceral fat and skeletal muscle of mice were detected.
0.72 PPARgamma and LPL Gene in a High-Fat Diet C57BL/6 Mice Model
31524223 0.98 PPARgamma, which is a key regulator of CD36, regulates lipid metabolism via activating LXRalpha and up-regulating ABCA1 expression.
0.98 CD36 mediates the endocytosis of oxLDL, activates the PPARgamma-LXRalpha-ABCA1 pathway, promotes the reverse transportation of excess cholesterol to HDL, accelerates the process of RCT and exerts atheroprotective effects.
0.97 CD36, PPARgamma, LXRalpha and ABCA1.
0.97 CD36 protein expression and the upregulation of PPARgamma, LXRalpha and ABCA1 protein expression levels in both the aortic and liver tissue.
0.97 CD36, PPARgamma, LXRalpha and ABCA1.
0.96 CD36), peroxisome proliferator-activated receptor gamma (PPARgamma), liver X receptor alpha (LXRalpha) and ATP binding cassette transporter A1 (ABCA1).
0.96 CD36 were upregulated, while the expression levels of PPARgamma, LXRalpha and ABCA1 were downregulated in both the aorta and liver.
0.94 CD36, PPARgamma, LXRalpha and ABCA1
0.94 CD36 expression levels increased, while those of PPARgamma, LXRalpha and ABCA1 decreased in both the aorta and liver tissue.
0.90 CD36 were increased, while those of PPARgamma, LXRalpha and ABCA1 were decreased in the aortas and livers of the model group mice.
0.87 PPARgamma, LXRalpha and ABCA1 protein levels (P<0.05, P<0.01 and P<0.001) and significant decreases in PCSK9 and CD36 protein levels (P<0.05, and P<0.01) as compared with the model group.
0.84 PPARgamma, LXRalpha and ABCA1 decreased (P<0.5 and P<0.01), while those of PCSK9 and CD36 increased (P<0.05 and P<0.001) in both the aorta and the liver as compared with the control group.
0.81 PPARgamma, LXRalpha and ABCA1 were high, while those of PCSK9 and CD36 were low in both the aorta and the liver.
22405074 0.98 PPARgamma (peroxisome proliferator-activated receptor-gamma) by synthetic ligands induces a brown fat-like gene program in WAT.
0.98 PPARgamma and PPAR-response elements (PPREs) on the promoter and/or enhancer of brown fat-selective genes.
0.98 PPARgamma is expressed abundantly and equally in white fat and brown fat, and is required for the development of both cell types.
0.98 PPARgamma ligands require full agonism to induce a brown (beige/brite) fat gene program in subcutaneous WAT and they do so through the activation of the PRDM16 pathway.
0.98 PPARgamma ligand drugs, such as rosiglitazone, have been shown to have the ability to turn on a thermogenic gene program in brown fat and activate a "browning" of white adipose tissues.
0.98 PPARgamma agonist activates a brown fat phenotype in a PRDM16-dependent manner.
0.97 fat (beige/brite) gene program together with the PPARgamma agonist.
0.92 PPARgamma is required to activate a thermogenic brown fat gene program in subcutaneous white fat
0.92 PPARgamma ligands on brown fat-selective gene expression were correlated with classical receptor transcriptional agonism per se.
0.78 PPARgamma ligands with weak agonism, at doses well above their respective KDs, had very modest or no effects on the expression of these brown fat-selective genes.
0.69 fat conversion achieved through PPARgamma ligands in closer detail.
0.65 PPARgamma in white adipocytes does not induce a white-to-brown fat conversion.
21480322 0.98 fat diet-induced hepatic steatosis as well as PPARgamma-stimulated adipogenic hepatic steatosis.
0.98 fat diet in MED1fl/fl mice was not associated with induction of PPARgamma target gene aP2 but this protein was detected in PPARgamma-induced hepatic adiposis (Fig. 1C).
0.98 fat diet-induced (Fig.1) and PPARgamma-stimulated hepatic steatosis (Fig.2).
0.97 fat diet induced as well as PPARgamma-stimulated gene expression and points to a new layer of regulatory complexity in the development of hepatic steatosis.
0.97 PPARgamma is not activated in steatotic livers resulting from high-fat diet feeding as evidenced by the failure of induction of aP2 expression in such livers and yet high-fat diet induced steatosis appears to be dependent on MED1.
0.97 PPARgamma is not activated in liver upon high fat feeding, then MED1 has significant PPARgamma-independent effects on hepatic steatosis.
0.97 Fat droplet proteins S3-12 (perilipin-4) and CideA , while they were strongly induced in MED1fl/fl mice, are barely detected in PPARgamma overexpressing MED1DeltaLiv mouse liver (Fig. 4B-D).
0.96 fat diet feeding as well as by PPARgamma overexpression is markedly attenuated (Fig. 2).
0.96 fat diet-induced and PPARgamma-induced hepatic steatosis and that loss of MED1 protects against fatty liver under these conditions.
0.94 fat diet-induced and PPARgamma-stimulated fatty liver development, which suggest that MED1 may be considered a potential therapeutic target for hepatic steatosis.
0.91 PPARgamma-stimulated adipogenic hepatic steatosis, we used in this study genetically altered mouse lineages and demonstrate that deletion of MED1 in mouse liver (MED1DeltaLiv) impairs high-fat diet-induced and PPARgamma-stimulated hepatic steatosis, whereas deficiency of coactivators such as SRC-1, PRIC285, PRIP, and PIMT had no effect.
26475357 0.98 Peroxisome proliferator activated receptor gamma (PPAR-gamma) is a ligand activated transcription factor which is regarded as a master regulator of fat deposition.
0.98 fat tissue and significantly decreased the fat deposition, which was associated with a significant down-regulation of PPAR-gamma protein content and an activation of lipolytic genes.
0.97 fat after miR-130b-MV injection while the protein content of its target gene PPAR-gamma was significantly suppressed, together with a significant up-regulation of the lipolysis genes, hormone sensitive lipase, monoglyceride lipase and leptin.
0.97 PPAR-gamma can stimulate lipogenesis and adipogenesis, while down-regulation of PPAR-gamma decreases fat mass in mice.
0.97 fat deposition in high-fat diet-induced obese mice in vivo, at least partly through the translational repression of PPAR-gamma.
0.97 PPAR-gamma, are also predicted to be the target of miR-130b, yet the mRNA expression of these genes in the epididymal fat tissue was not affected by miR-130b-MV treatment.
0.97 fat tissue to down-regulate PPAR-gamma expression and to stimulate the expression of lipolysis genes.
0.96 fat deposition and partly restore glucose tolerance, through translational repression of PPAR-gamma in a high-fat diet-induced obese mouse model.
0.96 fat deposition, miR-130b and its target gene PPAR-gamma expression.
0.95 PPAR-gamma was significantly reduced (P < 0.05) in the epididymal fat of mice injected with miR-130b-MV (Fig. 3k).
0.93 fat deposition through targeting PPAR-gamma in vivo.
23895241 0.98 PPARgamma (peroxisome proliferator-activated receptor gamma) and PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator 1alpha), which have been shown to be the key nodes in the regulation of inducible brown fat.
0.98 PPARgamma (peroxisome proliferator-activated receptor gamma) agonist or beta-adrenergic stimulation, a brown-fat-like gene expression program [e.g. UCP1, Cidea (cell death-inducing DFFA-like effector a) and Dio2 (diodinase 2)] is induced in a subset of Myf5- adipocytes in WAT.
0.98 PPARgamma is required to induce the brown-fat gene programme in subcutaneous WAT in mice, and PRDM16 (PR domain containing 16) is required for this process (Figure 1, and see the PRDM16 section for details).
0.98 PPARgamma binding sites in primary interscapular BAT and epididymal WAT, EBF2 (early B cell factor-2) was identified as the cofactor that regulates PPARgamma binding activity to brown rather than white-fat genes.
0.98 PPARgamma was shown to be involved in both the former and the latter: mutation of PPARgamma ligand binding site prevents troglitazone-associated inhibition of white-fat genes in 3T3-L1 adipocytes.
0.98 fat-selective cofactor, TLE3, which promotes lipid storage by blocking the interaction of PRDM16 with PPARgamma.
0.98 fat development: PRDM16, PPARgamma and PGC-1alpha (Figure 1).
27034954 0.98 PPARgamma, along with the liver X receptor (LXR) and pregnane X receptor (PXR), was found to be an upstream regulator of CD36; the presence of PPARgamma, LXR, and PXR binding sites in the Cd36 promoter was previously identified.
0.97 PPARgamma) nuclear translocation and increased levels of cell-surface CD36.
0.97 PPARgamma- and CD36-dependent lipid uptake, TAG synthesis, and lipid droplet formation.
0.97 PPARgamma, as well as by inducing the expression of downstream genes including Cd36, Dgat2, and Plin2 to increase lipid uptake, TAG synthesis, and lipid droplet formation in hepatocytes.
0.95 PPARgamma- and CD36-regulated lipid metabolism in VPA-induced hepatic steatosis.
0.95 CD36, DGAT2, and PLIN2 in liver is previously known to be regulated by PPARgamma, a crucial nuclear transcription factor controlling cellular glucose and lipid metabolism, we also investigated whether PPARgamma is involved in VPA-induced hepatic steatosis.
0.86 PPARgamma was previously reported to upregulate the expression of Plin2, Cd36, and many other steatotic genes in liver, we evaluated the mRNA, protein expression levels, and protein nuclear translocation of PPARgamma in FL83B cells under VPA treatment.
17389766 0.98 PPARgamma to regulate genes expressed in both brown and white adipocytes, but also the brown fat-specific UCP1 gene .
0.98 fat-like" features by thiazolidinediones entails direct upregulation of transcription of the PGC1alpha gene by PPARgamma in adipocytes.
0.98 PPARgamma or PPARalpha can induce UCP1 gene expression both in brown fat "in vivo" and in brown adipocytes "in vitro".
0.98 PPARgamma in the liver under basal conditions, it is increased in obesity, in insulin resistance, and after a high-fat diet.
0.98 PPARgamma is highly expressed in liver from PPARalpha null-mice fed a high-fat diet, and this is associated with an induction of UCP2 gene expression.
0.98 PPARgamma and coactivation by PGC-1alpha, in concert with overall induction of adipocyte differentiation towards the brown fat lineage.
22142492 0.98 fat accumulation in the aP2Spry-KO was associated with increased expression of adipogenic markers PPAR-gamma and FABP4 (Fig. 1D).
0.98 PPAR-gamma (Fig. 1G) and FABP4 (Fig. 1H) both on a normal and a high fat diet.
0.98 fat tissue has dual consequences, 1) inhibiting adipocyte differentiation mediated by PPARgamma inhibition and 2) inhibiting adipose tissue mediated angiogenesis resulting in decreased macrophage infiltration and inflammation in the adipose tissue.
0.95 fat diet induced bone loss is complex and could involve several factors: 1) lineage allocation of MSCs; 2) RANKL induced bone loss from immune cell activation; 3) bone resorption from activation of PPARgamma and 4) direct effects of free fatty acids on bone formation.
0.95 PPARgamma activation of bone resorption and therefore prevent high fat diet-induced bone loss.
0.91 PPARgamma and therefore may cause little change with a high fat diet but could still impact bone mass through non-cell autonomous effects on osteoblasts.
23473036 0.98 PPARgamma is the master transcriptional regulator of white and brown fat differentiation, and mice deficient in PPARgamma lack both types of adipose tissue.
0.98 PPARgamma to facilitate brown fat-selective gene expression.
0.98 fat-selective transcriptional program through direct interaction with PPARgamma.
0.97 fat program and promotes lipid storage by blocking the interaction of Prdm16 with PPARgamma, thereby reducing the occupancy of Prdm16 on brown fat-selective genes.
0.94 fat is a "default" transcriptional program that is executed by PPARgamma in the absence of Prdm16 and PGC-1alpha, or whether there are white fat-selective counterparts to these brown-selective cofactors.
0.94 fat is simply a "default" transcriptional program that is executed by PPARgamma in the absence of Prdm16 and PGC-1alpha, or whether there are white fat-selective counterparts to these brown-selective cofactors.
27138164 0.98 peroxisome proliferator-activated receptor-gamma (PPARgamma) by full agonists, such as thiazolidinediones (TZDs), has been shown to drive browning of WAT by stabilizing PRD1-BF-1-RIZ1 homologous domain-containing protein-16 (PRDM16), a transcriptional coregulator that was previously shown to control the development of genuine brown fat from myoblastic-like precursors.
0.98 PPARgamma agonists preferentially occurs in subcutaneous over visceral white fat depots and is largely due to stabilization and increased levels of Prdm16, a transcriptional regulator implicated in brown fat and also in beige adipocyte development.
0.95 PPARgamma Agonist, Induces the Expression of Thermogenesis-Related Genes in Brown Fat and Visceral White Fat and Decreases Visceral Adiposity in Obese and Hyperglycemic Mice
0.94 PPARgamma agonist, the TZD-derivative GQ-16, that is less adipogenic in cell culture and in vivo, and reverses high fat diet-induced insulin resistance and glucose intolerance similarly to RSG in mice but without inducing weight gain.
0.92 PPARgamma agonists does not translate into increased adaptive thermogenesis and energy expenditure, in keeping with TZD's effect of inducing increased metabolic efficiency, increased fat mass and weight gain.
0.90 fat depots not analysed herein, such as the mesenteric, retroperitoneal or anterior subcutaneous, would respond to PPARgamma activation in this mouse strain.
28934139 0.98 PPARgamma is a first inducer of fat cell development and promotes adipogenesis by co-expression with C/EBPalpha.
0.97 fat tissues, supplementation with stevioside or phyllodulcin significantly decreased mRNA expression of lipogenesis-related genes, including CCAAT/enhancer-binding protein alpha (C/EBPalpha), peroxisome proliferator activated receptor gamma (PPARgamma), and sterol regulatory element-binding protein-1C (SREBP-1c) compared to the high-fat group.
0.97 PPARgamma and C/EBPalpha, in intraperitoneal and extraperitoneal fat.
0.96 fat by downregulating C/EBPalpha, PPARgamma, and SREBP1c.
0.90 peroxisome proliferator activated receptor gamma (PPARgamma), and sterol regulatory element-binding protein-1C (SREBP-1c) were analyzed to investigate the effect of phyllodulcin on adipogenesis and lipogenesis in subcutaneous fat (Figure 2B).
0.68 PPARgamma are involved in the differentiation of both white and brown fat; this possibility should be determined in a future study.
31964951 0.98 Fat accumulation in the liver is generally caused by increased lipotoxicity resulting from high levels of free fatty acids, free cholesterol, and lipid metabolites, and these, in turn, are regulated by lipogenic genes, such as PPARgamma, C/EBPalpha, FAS, and FABP4.
0.98 fat oxidation by regulating the expression of PPARgamma in HFD-induced obese rodents.
0.96 PPARgamma, HSL, SCD-1, and FAT/CD36 in the liver, resulting in the reduction of body weight and fat volume in HFD-fed obese mice.
0.95 PPARgamma and HSL, resulting in reduced body fat and liver weight in HFD-induced obese mice.
0.93 PPARgamma and HSL in the liver, resulting in the reduction of body weight and fat volume in HFD-fed mice.
0.69 PPARgamma (0.2 +- 0.1 in NCD group, 0.7 +- 0.2 in HFD group, and 0.3 +- 0.1 in LMT1-48 group), HSL (0.9 +- 0.2 in NCD group, 1.3 +- 0.3 in HFD group, and 0.6 +- 0.2 in LMT1-48 group), SCD1 (0.4 +- 0.2 in NCD group, 1.2 +- 0.4 in HFD group, and 0.2 +- 0.1 in LMT1-48 group), and FAT/CD36 (0.2 +- 0.0 in NCD group, 1.2 +- 0.1 in HFD group, and 0.2 +- 0.1 in LMT1-48 group) in the livers of HFD-fed mice (Fig. 3C-F).
20374957 0.98 fat differentiation had previously identified PPARgamma (peroxisome proliferator-activated receptor-gamma) and the C/EBPs (CCAAT/enhancer-binding proteins) as key transcription factors driving fat cell differentiation (reviewed in).
0.98 fat cells as a cold-inducible co-activator of PPARgamma.
0.97 fat cell differentiation requires PPARgamma but, importantly, this factor alone is not sufficient to drive mesenchymal cells into a brown fat program.
0.97 PPARgamma and PGC-1alpha, which then drives a brown fat differentiation program.
0.95 PPARgamma is absolutely necessary for both white fat and brown fat cell development.
22933117 0.98 PPARgamma and C/EBPalpha act as adipogenic transcription factors during adipocyte differentiation, they are lipolytic in sum in differentiated adipocytes and are downregulated by ALK7 in obesity to accumulate fat.
0.98 peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein (C/EBP) alpha and promotes lipolysis by increasing the expression of adipose lipases, which leads to a net decrease in fat accumulation.
0.98 PPARgamma and C/EBPalpha play a pivotal role in the lipid remodeling of mature adipocytes and that their dysfunction leads to decreased mobilization of TG and increased fat accumulation in adipocytes.
0.97 PPARgamma and C/EBPalpha induce net lipolysis and decrease fat mass in sum in mature adipocytes.
0.90 Fat in Obesity Through Downregulation of Peroxisome Proliferator-Activated Receptor gamma and C/EBPalpha
24810249 0.98 fat phenotype in mesenchymal cells are mediated through PPARgamma, as well as TEL activity to antagonize the negative effect of ROSI on both osteoblast phenotype and TGFbeta/BMP signaling pathway.
0.97 PPARgamma fat "beiging" properties resulting from lysine deacetylation.
0.97 PPARgamma protein, our data suggest that Ser112 can be involved in the process of fat "beiging".
0.96 fat and an absence of anti-osteoblastic activity of PPARgamma, whereas low levels of Ser112pPPARgamma upon ROSI treatment correlated with lipid accumulating pro-adipocytic and anti-osteoblastic activities of PPARgamma.
0.61 PPARgamma fat "browning" activity and a lack of anti-osteoblastic activity.
24840660 0.98 PPARgamma-1/2 in the nucleus of apoER2-deficient RAW 264.7 macrophages also resulted in elevated mRNA levels of PPARgamma-responsive genes such as Cd36, Lrp1, and Abca1 in comparison to the levels observed in control cells (Figs. 2B and 6B).
0.98 Cd36, another PPARgamma-responsive gene that is known to promote atherosclerosis.
0.97 PPARgamma expression and its induction of p53 phosphorylation, and that this mechanism is independent of PPARgamma-induced CD36 expression.
0.94 PPARgamma-responsive gene CD36 was up-regulated in the apoER2-deficient macrophages, which likely resulted in the increased neutral lipid accumulation observed in these cells, we also determined if inhibiting CD36-mediated oxLDL uptake also desensitized the apoER2-deficient macrophages to oxLDL-induced cell death.
0.91 PPARgamma, but not CD36, Partially Rescues the ApoER2-deficient Macrophage Phenotype
24876128 0.98 PPARgamma and UCP1) and mRNA (Pgc1alpha, Ucp1, and Cidea) levels of brown adipocyte markers become significantly reduced 5 days post-induction, suggesting an efficient blockade of brown fat differentiation (Figure 2C,D).
0.98 Fat-TFIID has gained the ability to bind endogenous PPARgamma, which we speculate might facilitate its association with distinct cofactors such as PRDM16 in BAT or TLE3 in WAT to differentially regulate brown and white adipocyte formation.
0.98 fat-specific transcription factor PPARgamma (Figure 3E).
0.97 Fat-TFIID associates with PPARgamma and facilitates DNA looping formation.
0.87 PPARgamma co-purifies with TAF7L in the Fat-TFIID complex from differentiated C3H10T1/2 cells but not from control FLAG-V5-GFP cells (Figure 3A,B) nor with canonical TFIID lacking TAF7L (data not shown).
26775807 0.98 PPARgamma plays a critical role in adipocyte differentiation and fat deposition, which is expressed predominantly in adipose tissue and liver tissue.
0.96 fat through the inhibition of PPARgamma transcription activity.
0.96 fat droplets and improved liver morphology in DIO mice in a similar fashion to other PPARgamma antagonists, suggesting that isorhamnetin can be used to prevent hepatic steatosis.
0.95 PPARgamma agonist rosiglitazone, reduced obesity development and ameliorated hepatic steatosis induced by both high-fat diet treatment and leptin deficiency.
0.88 PPARgamma-dependent adipocyte differentiation, we next investigated the effect of isorhamnetin on obesity and metabolic disorders induced by high-fat diet.
27110487 0.98 PPARgamma (Rosi) or PPARalpha (GW) agonists added for 4 days on differentiated white adipocytes (Figure S1A) increased UCP1 mRNA and protein levels (15- and 11-fold increase, respectively) (Figure 1A,B), as well as expression of genes classically elevated in brown and brite fat cells (CIDEA, CPT1b, ELOVL3, PGC1alpha) (Figure 1A).
0.98 PPARgamma and PPARalpha have well established roles in driving adipogenesis/triglyceride storage and fatty acid oxidation, respectively, in fat cells.
0.96 PPARgamma or PPARalpha activation, hMADS white adipocytes display a molecular pattern of brite fat cells.
0.95 PPARgamma role in brown fat cell differentiation has been extensively studied.
0.60 fat cells was induced with selective PPARgamma and PPARalpha agonists to investigate fat and glucose metabolism.
18302760 0.98 peroxisome proliferator-activated receptor gamma (PPARgamma) resulted in an up-regulation of the CD36 scavenger receptor.
0.98 PPARgamma as a transcriptional regulator of CD36 gene expression has been previously established.
0.98 CD36 gene expression, authors suggested that the transcriptional regulators PPARgamma and Nrf2 may interact functionally to modulate CD36 gene expression.
0.96 PPARgamma seems to be determinant in the CD36 gene regulation as deduced from macrophages derived from mice in which the PPARgamma gene has been "floxed out".
18317516 0.98 fat regulator PPARgamma (96).
0.96 PPARgamma, PPARalpha, and PPARbeta/delta, which would lead to downregulation of fat metabolism.
0.96 fat depot changes came from the study showing that old animal preadipocytes expressed less PPARgamma.
0.96 PPARgamma activity and because PPARgamma activity helps determine age-related insulin resistance, SIRT1 may have an important role in metabolic diseases and link the effects of food consumption to body fat mass and diseases of aging.
20101262 0.98 PPARgamma is both sufficient and necessary for the differentiation of white fat adipocytes.
0.98 PPARgamma-controlled differentiation of white fat adipocytes involves a transcriptional cascade that includes members of C/EBP transcription factors (Figure 1A).
0.98 PPARgamma can be co-activated by PRDM16 and PGC-1, does PPARgamma directly regulate expression of some brown-fat specific genes through these co-activators?
0.91 PPARgamma alone generates a fat phenotype that is common to both WAT and BAT.
23525438 0.98 peroxisome proliferator-activated receptor-gamma (PPARgamma) induces expression of fatty acid-binding protein 4 (FABP4) and fatty acid translocase (FAT)/CD36 in capillary endothelial cells (ECs) to promote FA transport into the heart.
0.95 PPARgamma are likely to be involved in FA uptake in combination with FABP4 and FAT/CD36.
0.94 Pparg EC/null mice as compared with Ppargfl/null mice after olive oil loading, whereas those values were comparable between Ppargfl/null and Pparg EC/null null mice on standard chow and a high-fat diet.
0.85 PPARgamma deficiency in ECs caused marked dyslipidemia after a high-fat diet or olive oil gavage.
25586556 0.98 PPARgamma activity and expression of its target molecules, including CD36, macrophage mannose receptor, and arginase 1, were persistently enhanced following apoptotic cell instillation.
0.98 PPARgamma targets, including CD36, MMR, and Arg1, in alveolar macrophages and lung tissue following apoptotic cell instillation was greater than that observed following bleomycin with or without viable cells.
0.98 PPARgamma expression and activity, in turn, regulates the macrophage program of alternative activation with increased efferocytic surface receptors, including the PPARgamma target molecules, CD36, MMR, and Arg1.
0.96 PPARgamma functional activity, we examined the expression of CD36, macrophage mannose receptor (MMR), and arginase 1 (Arg1), all of which are upregulated by PPARgamma and characteristic of alternative macrophage programming.
26085100 0.98 fat accumulation in CBA mice was paralleled by an increase in the hepatic expression of Ppargamma and the Ppargamma target genes Cd36, Fabp4, and Mogat1, i.e. genes involved in FA uptake and TG synthesis.
0.98 Ppargamma, and in particular Ppargamma2, overexpression promotes hepatic fat accumulation in an Srebp-1c independent way, whereas a liver-specific deletion of Ppargamma attenuates hepatic steatosis, highlighting the important role for Ppargamma in fatty liver development.
0.97 Ppargamma target genes, such as the intracellular FA chaperone fatty acid-binding protein 4 (Fabp4) and monoacylglycerol acetyltransferase (Mogat1), which enhances hepatic fat accumulation by stimulating incorporation of FAs into TG via a FA biosynthesis-independent pathway, was also increased in livers of CBA mice at 3w of SRD (Fig. 5, C and D), whereas hepatic Mogat1 and Fabp4 expression was unaltered in 3w SRD B6 mice (Fig. 5E).
0.70 fat accumulation, and dysglycemia in B6 mice, and hepatic expression of Ppargamma, Cd36, Fabp4, and Mogat1 was not increased SRD B6 mice.
27799461 0.98 PPARgamma knockout models have led to the conclusion that PPARgamma directly promotes hepatic fat accumulation by increasing lipid uptake, as well as promoting DNL.
0.98 PPARgamma, that could explain why aLivPPARgammakd protects against hepatic fat accumulation.
0.95 PPARgamma transgene in the liver of HF-fed PPARalpha knockout or WT mice dramatically increases hepatic fat content; 3) congenital hepatocyte-specific knockout of PPARgamma reduces hepatic fat content in mice fed a high-fat (HF) diet, as well as in mice with fatty liver due to inactivating mutations in the leptin gene [ob/ob; ] or lipodystrophy induced by lack of adipocyte development [AZIP ].
0.87 PPARgamma promotes liver fat accumulation by regulating the expression of genes important for DNL, aLivPPARgammakd did not significantly reduce the expression of DNL genes (Srebp1c, Acc1, Fasn, Elov6, Scd1) across age or diet.
30037087 0.98 PPARgamma is predominantly expressed in adipose tissues, both white and brown, where it plays an important anabolic role in facilitating fat storage, adipogenesis, and thermogenesis.
0.98 PPARgamma activation facilitates fat accretion and retains the functionality of adipose tissue by coordinating adipogenesis, fat transport, and lipolysis upon reaching an individualized threshold of adipose tissue mass.
0.98 PPARgamma is necessary for fat cell differentiation in all adipose depots and contributes to define the maximum threshold of expansion of the WAT.
0.97 fat phenotype in the WAT by CR or PPARgamma agonists would result in an increased mitochondrial functionality with beneficial effects on aging and metabolism.
30987673 0.98 PPARgamma protein levels in gonadal fat (Additional file 4 E).
0.97 PPARgamma in the brown fat of male mice, the results suggest Siah2-mediated regulation of select nuclear receptor protein levels depends on signaling events that are both fat depot-specific and sex-dependent.
0.97 PPARgamma protein expression contrasts with the effect of Siah2 deficiency on PPARgamma protein levels in white fat of HFD-fed obese male mice and (Additional file 4 E), suggesting both sex- and fat depot-specific effects of Siah2 in nuclear receptor protein levels.
0.94 fat did not depend on AMPK signaling in brown fat, and unexpectedly, loss of Siah2 in the HFD-fed female brown fat substantially reduced expression of ERalpha and ERRgamma proteins while reductions in PPARgamma protein levels were not statistically significant.
17259664 0.98 PPAR-gamma are ligand-selective, suggesting the existence of multiple mechanisms by which PPAR-gamma controls bone mass and fat mass in bone.
0.96 PPAR-gamma transcription factor is essential for both extramedullary and bone marrow fat development , yet bone marrow adipocyte biology and function are not well understood.
0.95 PPAR-gamma gene exhibits both decreased marrow fat content and increased bone mass.
20149618 0.98 PPARgamma accounts for increased BM fat and decreased production of osteoblasts related to aging.
0.97 PPARgamma in subcutaneous fat tissue is lower in older monkeys than young and mutations of the PPARgamma gene are associated with an altered balance between bone and fat formation in the marrow.
0.91 PPARgamma pathway is also associated with fat redistribution and bone loss related to aging.
22916336 0.98 PPARgamma and PPARdelta reduce fatty acid efflux by promoting fat storage or burning, respectively (Fig. 4).
0.97 PPARgamma deletion in macrophages is associated with impaired glucose tolerance and insulin resistance in response to a high fat diet.
0.97 PPARgamma activation reduces fatty acid efflux by promoting fat storage and increasing adiponectin production, which improves systemic lipid and glucose metabolism.
23700465 0.98 FAT)/CD36, a PPARgamma target gene, is involved with long chain fatty acid (LCFAs) transport into mitochondria, correlating with oxidative capacity of the liver as long as CPT-1 is also present.
0.95 fat pad mass distribution, higher numbers of larger adipocytes, hepatic steatosis, high mRNA expression of lipogenic proteins and its target genes concomitant to decreased expression of PPARalpha and CPT-1 in liver, and diminished expression of PPARgamma and adiponectin in WAT.
0.94 fat pad mass distribution, higher number of larger adipocytes, hepatic steatosis, higher expression of lipogenic proteins concomitant to decreased expression of PPARalpha and carnitine palmitoyltransferase I (CPT-1) in liver, and diminished expression of PPARgamma and adiponectin in WAT.
24772164 0.98 PPARgamma and its adipocyte-specific target genes (aP2, CD36/FAT).
0.95 PPARgamma2 in the subcutaneous adipose tissue were associated with high liver fat content, as well as with insulin resistance.
0.87 PPARgamma2 expression and hepatic fat content.
25128964 0.98 fat cells, including peroxisome proliferator-activated receptor gamma (PPARgamma), CCAAT/enhancer binding protein (C/EBP, which includes C/EBP alpha, C/EBP beta, and C/EBP delta), adipocyte lipid binding protein (ALBP), and adipocyte determination and differentiation factor 1 (ADD1).
0.98 PPARgamma is most specific to fat cells and exerts the strongest effect in adipogenesis.
0.98 PPARgamma was important in brown fat metabolism, along with some other transcription factors including PPARalpha, ERRalpha, NRF1, and PGC-1alpha.
25143786 0.98 fat feeding activates protein kinase cdk5 which in turn phosphorylates PPARgamma at Serine 273 in adipose tissues.
0.98 fat diet induced CDK5 mediated phosphorylation of PPARgamma is reported to dysregulate expression of a number of genes including adiponectin.
0.97 PPARgamma at Serine 273 was markedly increased in adipocytes from both mesenteric and inguinal fat depots while in adipocytes from the same depots it was very significantly reduced in the CNX-013-B2 treated animals (Figure 6A, B).
26280538 0.98 PPARgamma-specific transcriptional programs, suggesting C/EBPalpha is regulating mostly pathways modulated by high dietary fat exposure.
0.89 fat cells, compared to 298 genes altered when PPARgamma is deleted.
0.75 PPARgamma deletion, the overall structure and viability of the fat pad is negatively affected, which is consistent with a recent publication by the group of Lazar.
27552974 0.98 PPARgamma agonists) also induce a brown-fat-like program in mouse and human WAT-derived adipogenic precursor cells.
0.98 PPARgamma specifically in smooth muscle cells results in a complete loss of perivascular adipocytes that are known to have a cold-inducible beige fat profile.
0.98 PPARgamma; ZFP516 and EHMT1; (4) EBF2 cooperates with PPARgamma to activate the brown fat-selective program.
32245957 0.98 Pparg, and Ucp1 transcripts, which leads to a marked reduction in BAT-mediated adaptive thermogenesis and promotes high-fat diet (HFD)-induced obesity and systemic insulin resistance.
0.98 PPARgamma are early key transcriptional factors in the fate-determination of brown fat.
0.98 fat related genes, including Prdm16, Pparg, Pgc-1alpha, and Ucp1.
17389767 0.98 PPARgamma in livers of PPARalpha -/- mice fed a high-fat diet leads to increased expression of adipocyte markers and might contribute to the fatty liver phenotype .
0.98 fat diet were strongly downregulated by PPARgamma overexpression in liver.
19345188 0.98 fat cells with the PPARdelta agonist, but not the agonist for PPARgamma or PPARalpha, induced twist-1 expression (Figure 7A).
0.97 PPARgamma, binds to the twist-1 promoter, and directs twist-1 expression both in brown fat cell culture and in whole animals, suggesting a feedback regulatory mechanism.
20831792 0.98 Ppar-gamma is down-regulated despite high body fat mass and increased adipocyte size in comparison to B6.
0.95 Ppar-gamma expression seems to counteract fat accumulation rather than to promote fat storage.
24130751 0.98 PPARgamma2 and lipid droplet proteins FSP27 and CIDEA in the liver is dependent upon dietary fat.
0.97 Ppargamma2, Fsp27 and Cidea gene expression and the level of serum and hepatic TG in LFC-reared wild type and Gcn2 KO mice is similar (Fig. 3A-C) demonstrating that the HiS/LoH TG phenotype is dependent upon increased fat present in the MFC diet.
24793638 0.98 fat-specific PPARgamma deletion results in various abnormalities, including reduced white and brown fat, decreased adipocyte gene expression, and fatty liver and recently a more efficient fat-specific knockout revealed a critical role for adipocyte PPARgamma in all adipose depots including mammary gland, bone marrow, and skin.
0.96 PPARgamma knockout in mice is embryonic lethal due to placental defects, while mice with chimeric PPARgamma expression have shown that embryonic stem cells lacking PPARgamma cannot contribute to fat formation.
25101993 0.98 PPARgamma agonist, rosiglitazone, can rescue the effects of Sdc1 deficiency, and we conclude that Sdc1 is likely to be a component of the sensory trigger for intradermal fat differentiation.
0.93 fat in Sdc1-/- mice can be rescued by administration of the PPARgamma agonist, rosiglitazone, in vitro and in vivo.
25470547 0.98 PPARgamma in WAT of TRF mice is reminiscent of the protective role it plays by promoting the development of "better quality" fat tissue.
0.96 fat metabolism, namely PPARgamma.
19680557 0.98 fat is the transcriptional induction of nearly all aspects of lipid metabolism, including those regulated by PPARalpha (lipolysis, fatty acid beta-oxidation), PPARgamma (adipogenesis and adipogenic transformation, lipogenesis, lipid accumulation, lipid uptake) and SREBP1 (lipogenesis, fatty acid synthesis, fatty acid desaturation, fatty acid elongation) (Figure 2, 3, 5).
25754247 0.98 PPARgamma and recruiting other key enzymes to promote fat accumulation during aging.
27301785 0.98 PPARgamma dually modulates transcriptional activities of PPARalpha and PPARgamma and regulates brown fat adipogenesis and function.
28245284 0.98 PPARgamma preferentially directs lipid storage to subcutaneous adipose tissue, as the PPARgamma agonist rosiglitazone induces 2-fold more subcutaneous triglyceride storage than visceral fat storage.
25064526 0.97 fat diet, both of which potently activate the PPARgamma-RXR complex.
0.97 PPARgamma in bone metabolism and the central role of RXR in determining PPARgamma responses, essentially nothing is known about how specific retinoid pathways modulate PPARgamma-RXR action in bone and skeletal responses to other stimuli known to alter bone remodeling, like high fat diet (HFD) and TZDs.
0.97 PPARgamma-RXR transactivation, thereby offsetting known effects of high fat diet HFD and TZDs on bone density and marrow adiposity.
0.95 fat diet (HFD), which can activate PPARgamma, as well as PPARgamma-activating anti-diabetic thiazolidinediones (TZDs) have been linked to bone loss, marrow adiposity, and fractures .
0.92 fat diets, which are know to increase PPARgamma levels, have been linked with decreased skeletal integrity.
30842627 0.97 PPARgamma and its target genes, namely, PTEN and CD36, in TAMs isolated from primary tumors after ApoSQ injection compared to those isolated from control mice (Fig. 8a).
0.96 PPARgamma and its target molecules PTEN and CD36, as well as the PTEN protein level, but reduced the mRNA levels of Snai1 and Zeb1 (Fig. 6f-j), as well as the Akt phosphorylation level (Fig. 6k).
0.96 PPARgamma, PTEN, and CD36 mRNA or protein expression were also shown in TAMs isolated from primary tumors after ApoSQ injection.
0.95 PPARgamma (green, Fig. 7a, b), PTEN (green, Fig. 7e, f), and CD36 expression (green, Fig. 7h, i) upon ApoSQ injection.
0.95 PPARgamma (Fig. 7d), PTEN (Fig. 7g), and CD36 (Fig. 7j) expression in F4/80-positive cells (red) was also markedly enhanced by apoptotic cell injection, which reflects apparent PPARgamma, PTEN, and CD36 induction in tumor-associated macrophages (TAMs), as the F4/80-positive macrophage intensity was not different (Fig. 7c).
28436456 0.97 PPARgamma antagonists ameliorated high-fat diet (HFD)-induced obesity, insulin resistance and fatty liver disease by inhibiting lipogenesis.
0.96 PPARgamma-independent action on fat accumulation and lipogenesis in vivo, supporting the idea that CC could be a potential PPARgamma antagonist.
0.95 fat accumulation as well as improves glucose homeostasis, hepatic lipid, inflammation and fibrosis as a novel natural antagonist of PPARgamma.
0.92 PPARgamma activity could be beneficial to prevent and treat obesity and obesity-related metabolic diseases, and it may even be superior to activation in terms of obesity based on fat formation and lipogenesis.
23640498 0.97 PPARgamma and CD36 mRNA expression was specifically up-regulated in high fat diet-induced liver steatosis in mice .
0.94 PPARgamma2 was significantly elevated in high fat-fed SMS2 transgenic mice (2.1-fold, P<0.001), but suppressed in SMS2 KO mice (69%, P<0.001) (Table 3).
0.92 fat diet-induced triglyceride and free fatty acid accumulation in the liver; 4) SMS2 overexpression induces hepatic PPARgamma2 and its downstream genes, CD36 and FSP27 levels, while SMS2 deficiency reduces all these levels; 5) exogenous ceramide but not sphingomyelin or phosphatidylcholine suppresses PPARgamma2, CD36, and FSP27 expression levels, and 6) PPARgamma antagonist reduces triglyceride accumulation in mouse liver.
30338310 0.97 fat on cortical expression of Mfsd2a and Glut1, with protein expression increases in the cortical tissue that correspond to an increase in Ppar-gamma mRNA expression.
0.70 fat had a lower DeltaDeltaCt for Ppar-gamma compared with those fed 10% fat (41% fat: -0.33; 10% fat: -0.16; P = 0.0419), translating to higher-fold Ppar-gamma mRNA expression in the 41% fat compared with the 10% fat group [2(-DeltaDeltaCt) 41% fat: 1.26; 10% fat: 1.11].
0.54 Ppar-gamma mRNA levels differed with type and percentage of fat (Table 3).
20111017 0.97 Pparg2 mRNA levels were slightly higher in all three intra-abdominal fat depots and BAT (Figure 1b and Table 1).
0.96 Pparg2 expression decreased in all fat depots during fasting of lean mice and ob/ob mice by 61-81%.
21569430 0.97 fat droplets in C3H10 T1/2 cells and it had no significant impact on any gene expression levels, although Furuyashiki et al. reported that in 3T3-L1 cells PPARgamma and C/EBPalpha were down-regulated by tea catechins, like EGCG.
0.83 fat metabolism (Glut4, LPL, FAS, ACC1 and CPT-1beta) and of adipocyte differentiation markers (PPARgamma, C/EBPalpha, PPARalpha, aP2 and adiponectin) were determined in maturing C3H10 T1/2 cells.
27200103 0.97 PPAR-gamma and C/EBP-alpha mRNA levels in the epididymal fat pad.
0.82 PPARgamma, C/EBPalpha, and lipin-1 were determined in the epididymal fat pad.
29617644 0.97 PPARG, the master transcriptional regulator of adipogenesis, whose expression in individual cells correlates closely with lipid accumulation, as well as with expression of GLUT4, adiponectin, and other mature fat cell markers (Figures 1B, S1A-S1C).
0.97 PPARG cells display mature fat cell features and accumulate high levels of lipid.
19392647 0.97 PPARG exists in four isoforms, PPARG1-4; however, PPARG2 is fat specific and due to its extra 30 N-terminal amino acids may have enhanced transcriptional activity.
22596050 0.97 PPARgamma can regulate expression of each other in a positive feedback manner and since Cebpa is induced by standard IC in Vis fat, the blockade appears to be in the ability of C/EBPalpha to stimulate a normal increase in PPARgamma.
29187824 0.97 PPARgamma overexpression in transgenic mice contributed to cardiac dysfunction encompassing an increase in FAT/CD36 level, FA uptake and intracellular lipid accumulation with rosiglitazone treatment even aggravating the lipotoxic effects.
20574519 0.96 PPARgamma has been implicated in the induction of obesity by a high fat diet; however, the absence of an effect of the PPARgamma (S112A) on adiposity does not suggest that this is important mechanism for regulation of ATE genes in mice with variable diet-induced obesity.
0.88 PPARgamma with fat mass at 10 and 112 days of age were non-significant (R = -0.01 and 0.14, respectively) and showed only marginal significance with some of the genes of ATE (Figure 6).
0.85 fat chow diet for 5 weeks from weaning, the size of adipocytes is reduced and the expression of ATE genes is strongly suppressed, while PPARgamma expression is maintained at a stable level.
0.65 PPARgamma is unaffected by the dietary protocol as indicated by the regression data between PPARgamma and Fat at D10 and D112 (R = -0.01 and 0.14, respectively).
18719582 0.96 PPARgamma can convert myogenic cells into adipocytes but PRDM16 expression additionally commits cells to the brown fat fate.
0.89 PPARgamma function per se would always display a brown fat phenotype.
31408999 0.96 fat accumulation, PPARgamma and FABP4 were significantly increased in the KDM4B-knockout mice.
0.96 PPARgamma activity and the fat storage capacity of the adipocytes.
28081181 0.96 PPARgamma in epididymal fat tissue, and reduced epididymal fat accumulation in rats.
29704660 0.94 fat diet , albeit in close proximity to capillaries, were negative not only for Ppargamma but also for Sma, Pdgfrbeta, and the endothelial marker, isolectin Ib4 .
27631008 0.93 fat mobilization in white fat tissue by inhibiting PPAR gamma.
0.88 PPAR gamma, ROR alpha, and RXR alpha) in fat tissue at specific time points.
0.70 PPAR gamma, ROR alpha, and RXR alpha in liver and fat of atherosclerotic mice.
0.64 PPAR gamma, ROR alpha, and RXR alpha in mouse fat tissues.
17710237 0.93 PPARgamma activator gained more weight than obese vehicle controls and the weight gain could be completely accounted for by increased fat mass which was equivalent to the increase in caloric intake.
0.91 fat mass (FM) while a PPARgamma agonist increased BW and FM commensurate with increased food consumption.
0.91 PPARgamma agonists enhances the action of insulin and reduces serum glucose in subjects with T2DM, however, substantial body weight gain also occurs that is comprised of both fat mass and fluid volume.
26770990 0.93 PPAR agonists' treatment improved glucose tolerance and insulin sensitivity in high-fat diet-induced obese mice.
0.71 fat diet (HFD) or administration of PPAR agonists.
26740599 0.93 fat-fed mice, Gleevec improved insulin sensitivity without causing severe side effects associated with other PPARgamma-targeting drugs.
26833256 0.93 PPAR gamma dose-dependently in a high-fat induced obesity mice model.
19468288 0.92 fat and are immediately downstream of Ppargamma .
0.72 Ppargamma hyp/hyp mice with a partial loss of function mutation in the Ppargamma gene have high bone mass and little marrow fat .
0.56 fat network: leptin, Ppargamma (peroxisome proliferator activated receptor gamma), and osteocalcin.
26140591 0.86 PPARgamma in mouse fat is strain-selective and driven by SNPs
28217782 0.86 PPARgamma agonists such as rosiglitazone have shown efficacy in restoring subcutaneous fat depots in a small number of clinical trials but drug side effects, including increased incidence of heart attacks, will likely prevent their widespread adoption.
23840542 0.79 PPARgamma/LXRalpha Pathway in apoE-/- Mice Fed a High-Fat/High-Cholesterol Diet
31118835 0.64 fat droplets in the treated cells, as well as measuring major adipogenic transcriptional factors in adipogenesis pathways which include PPARgamma and C/EBPalpha gene expressions.
20195269 0.59 fat has higher basal levels of PPARgamma 1 and 2, and are more responsive to TZDs than visceral fat .
19687618 0.58 fat weights, lipid droplets in liver, and PPAR-gamma expression.
23747579 0.54 PPARgamma with the endothelial specific receptor tyrosine kinase-Cre (Tie2-Cre) did not affect PPARgamma expression in fat or adipose tissue mass.



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