scholarly journals Comparative Effects of Luteolin and Quercetin on Adipogenesis in 3T3-L1 Cells

2021 ◽  
Vol 11 (1) ◽  
pp. 65-72
Author(s):  
Satoru Sakuma ◽  
Midori Yabuuchi ◽  
Ayumi Yoshizumi ◽  
Yui Okajima ◽  
Yohko Fujimoto ◽  
...  
Keyword(s):  
Potent Inhibitor ◽  
Peroxisome Proliferator ◽  
Inhibitory Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fat Accumulation ◽  
Expression Levels ◽  
Enhancer Binding Protein ◽  
Mrna And Protein Expression ◽  
Lifestyle Related Diseases ◽  
Pparγ Expression

Purpose: Quercetin has been reported as a more potent inhibitor of fat accumulation than other flavonoids. However, little information is available regarding the strength and mechanism of the repressive action of luteolin on fat accumulation. Therefore, the aim of the present study was to evaluate the comparative effects of luteolin and quercetin on the differentiation of 3T3-L1 preadipocytes into mature adipocytes. Methods: 3T3-L1 preadipocytes were differentiated by treatment with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine in the presence of luteolin or quercetin. Alterations in triacylglycerol (TG) levels, lipid-filled adipocyte quantity, and the mRNA and protein expression levels of CCAAT-enhancer-binding protein α (C/EBPα) and peroxisome proliferator–activated receptor γ (PPARγ) were measured. Results: Both luteolin and quercetin reduced TG levels, the number of lipid-filled adipocytes, and the mRNA expression levels of C/EBPα and PPARγ; however, these effects occurred with lower concentrations of luteolin than quercetin. Conclusions: These results suggest that luteolin may be more potent than quercetin in inhibiting adipocyte differentiation. These effects may be explained by differences in the inhibitory effects of the two compounds on C/EBPα and PPARγ expression. This study suggests that luteolin might be a beneficial dietary supplement for obesity and lifestyle-related diseases.

In vitro interaction between resistin and peroxisome proliferator-activated receptor γ in porcine ovarian follicles

2016 ◽  
Vol 28 (3) ◽  
pp. 357 ◽  
Author(s):  
Agnieszka Rak-Mardyła ◽  
Eliza Drwal
Keyword(s):  
Protein Expression ◽  
Ovarian Follicle ◽  
Hormone Secretion ◽  
Ovarian Follicles ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pparγ Agonist ◽  
Mrna And Protein Expression ◽  
Pparγ Expression

In the present study, using real-time polymerase chain reaction and immunoblotting methods, we quantified the expression of peroxisome proliferator-activated receptor (PPAR) γ, PPARα and PPARβ in different sized ovarian follicles (small (SF), medium (MF) and large (LF) follicles) in prepubertal and adult pigs. In prepubertal pigs, PPARγ and PPARα expression was highest in LF; however, PPARβ expression did not differ among SF, MF and LF. In mature pigs, only protein expression of PPARγ and PPARα increased during ovarian follicle development. Following identification of very high levels of PPARγ expression in LF in prepubertal and adult pigs, using in vitro culture of ovarian follicles, we determined the effect of resistin at 0.1, 1 and 10 ng mL–1 on PPARγ mRNA and protein expression and the effect of rosiglitazone at 25 and 50 µM (a PPARγ agonist) on resistin mRNA and protein expression. Resistin increased PPARγ expression in ovarian follicles in both prepubertal and adult pigs, whereas rosiglitazone had an inhibitory effect on resistin expression. The role of PPARγ in regulating the effects of resistin on ovarian steroidogenesis was investigated using GW9662 (a PPARγ antagonist at dose of 1 μM). In these studies, GW9662 reversed the effect of resistin on steroid hormone secretion. The data suggest that there is local cooperation between resistin and PPARγ expression in the porcine ovary. Resistin significantly increased the expression of PPARγ, whereas PPARγ decreased resistin expression; thus, PPARγ is a new key regulator of resistin expression and function.

scholarly journals The Demethoxy Derivatives of Curcumin Exhibit Greater Differentiation Suppression in 3T3-L1 Adipocytes Than Curcumin: A Mechanistic Study of Adipogenesis and Molecular Docking

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1025
Author(s):  
Ahmed Alalaiwe ◽  
Jia-You Fang ◽  
Hsien-Ju Lee ◽  
Chun-Hui Chiu ◽  
Ching-Yun Hsu
Keyword(s):  
Molecular Docking ◽  
Fatty Acid Synthase ◽  
Structural Similarity ◽  
Mechanistic Study ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Peroxisome Proliferator Activated Receptor ◽  
Enhancer Binding Protein ◽  
Underlying Mechanisms ◽  
Amp Activated Protein Kinase

Curcumin is a known anti-adipogenic agent for alleviating obesity and related disorders. Comprehensive comparisons of the anti-adipogenic activity of curcumin with other curcuminoids is minimal. This study compared adipogenesis inhibition with curcumin, demethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC), and their underlying mechanisms. We differentiated 3T3-L1 cells in the presence of curcuminoids, to determine lipid accumulation and triglyceride (TG) production. The expression of adipogenic transcription factors and lipogenic proteins was analyzed by Western blot. A significant reduction in Oil red O (ORO) staining was observed in the cells treated with curcuminoids at 20 μM. Inhibition was increased in the order of curcumin < DMC < BDMC. A similar trend was observed in the detection of intracellular TG. Curcuminoids suppressed differentiation by downregulating the expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), leading to the downregulation of the lipogenic enzymes acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). AMP-activated protein kinase α (AMPKα) phosphorylation was also activated by BDMC. Curcuminoids reduced the release of proinflammatory cytokines and leptin in 3T3-L1 cells in a dose-dependent manner, with BDMC showing the greatest potency. BDMC at 20 μM significantly decreased leptin by 72% compared with differentiated controls. Molecular docking computation indicated that curcuminoids, despite having structural similarity, had different interaction positions to PPARγ, C/EBPα, and ACC. The docking profiles suggested a possible interaction of curcuminoids with C/EBPα and ACC, to directly inhibit their expression.

scholarly journals Growth Hormone Inhibits Apoptosis in Human Colonic Cancer Cell Lines: Antagonistic Effects of Peroxisome Proliferator Activated Receptor-γ Ligands

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3353-3362 ◽  
Author(s):  
Fausto Bogazzi ◽  
Federica Ultimieri ◽  
Francesco Raggi ◽  
Dania Russo ◽  
Renato Vanacore ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Colonic Cancer ◽  
Cancer Cell Lines ◽  
Peroxisome Proliferator ◽  
Signal Transducer ◽  
Peroxisome Proliferator Activated Receptor ◽  
Antiapoptotic Effect ◽  
Pparγ Expression ◽  
Colonic Cells

Abstract GH has antiapoptotic effects on several cells. However, the antiapoptotic mechanisms of GH on colonic mucosa cells are not completely understood. Peroxisome proliferator activated receptor-γ (PPARγ) activation enhances apoptosis, and a link between GH and PPARγ in the colonic epithelium of acromegalic patients has been suggested. We investigated the effects of GH and of PPARγ ligands on apoptosis in colonic cancer cell lines. Colonic cells showed specific binding sites for GH, and after exposure to 0.05–50 nm GH, their apoptosis reduced by 45%. The antiapoptotic effect was due to either GH directly or GH-dependent local production of IGF-1. A 55–85% reduction of PPARγ expression was observed in GH-treated cells, compared with controls (P &lt; 0.05). However, treatment of the cells with 1–50 μm ciglitazone (cig), induced apoptosis and reverted the antiapoptotic effects of GH by increasing the programmed cell death up to 3.5-fold at 30 min and up to 1.7-fold at 24 h. Expression of Bcl-2 and TNF-related apoptosis-induced ligand was not affected by either GH or cig treatment, whereas GH reduced the expression of Bax, which was increased by cig treatment. In addition, GH increased the expression of signal transducer and activator of transcription 5b, which might be involved in the down-regulation of PPARγ expression. In conclusion, GH may exert a direct antiapoptotic effect on colonic cells, through an increased expression of signal transducer and activator of transcription 5b and a reduction of Bax and PPARγ. The reduced GH-dependent apoptosis can be overcome by PPARγ ligands, which might be useful chemopreventive agents in acromegalic patients, who have an increased colonic polyps prevalence.

scholarly journals Flubendiamide Enhances Adipogenesis and Inhibits AMPKα in 3T3-L1 Adipocytes

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2950 ◽  
Author(s):  
Quancai Sun ◽  
Jie Lin ◽  
Yukui Peng ◽  
Ruichang Gao ◽  
Ye Peng
Keyword(s):  
Adipocyte Differentiation ◽  
Peroxisome Proliferator ◽  
Potential Influence ◽  
Peroxisome Proliferator Activated Receptor ◽  
Acetyl Coenzyme A ◽  
Enhancer Binding Protein ◽  
Triglyceride Content ◽  
Important Regulator ◽  
Amp Activated Protein Kinase ◽  
Acetyl Coenzyme A Carboxylase

Flubendiamide, a ryanoid class insecticide, is widely used in agriculture. Several insecticides have been reported to promote adipogenesis. However, the potential influence of flubendiamide on adipogenesis is largely unknown. The current study was therefore to determine the effects of flubendiamide on adipogenesis utilizing the 3T3-L1 adipocytes model. Flubendiamide treatment not only enhanced triglyceride content in 3T3-L1 adipocytes, but also increased the expression of cytosine-cytosine-adenosine-adenosine-thymidine (CCAAT)/enhancer-binding protein α and peroxisome proliferator-activated receptor gamma-γ, two important regulators of adipocyte differentiation. Moreover, the expression of the most important regulator of lipogenesis, acetyl coenzyme A carboxylase, was also increased after flubendiamide treatment. Further study revealed that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or A769662, two Adenosine 5′-monophosphate (AMP)-activated protein kinase α activators, subverted effects of flubendiamide on enhanced adipogenesis. Together, these results suggest that flubendiamide promotes adipogenesis via an AMPKα-mediated pathway.

Abstract WP154: The Role of Ethylmethylhydroxypyridine Succinate in the Induction of PGC-1α in Experimental Ischemic Damage of the Prefrontal Cortex

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Fatima Shakova ◽  
Yuliya Kirova ◽  
Elita Germanova ◽  
Galina Romanova
Keyword(s):  
Prefrontal Cortex ◽  
Antioxidant Defense System ◽  
Peroxisome Proliferator ◽  
Ischemic Damage ◽  
Infarct Zone ◽  
Respiratory Enzymes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Expression Levels ◽  
Ethylmethylhydroxypyridine Succinate ◽  
Intact Rats

The aim of the study was to identify the potential succinate/SUCNR1-mediated mechanism of induction and activation of transcription coactivator PGC-1α (peroxisome proliferator-activated receptor-gamma coactivator 1 alpha) – key activator of the mitochondriogenesis, angiogenesis, fusion of mitochondria, antioxidant defense system that are basis of neuroprotective mechanisms – in the peri-infarction zone of the rat prefrontal cortex (PFC). Focal bilateral damage of the PFC was modeled by photo-induced thrombosis. Ethylmethylhydroxypyridine succinate (a form of succinate passing through the blood-brain barrier; trade name of the drug Mexidol) was injected intraperitoneally 2 hours after infarction and then every day at a dose of 100 mg/kg (7 day course). The tissue of the peri-infarction zone was taken 1, 3, 7 days after the start of therapy, as well as 14 days after discontinuation of the drug. Brain samples were stored in liquid nitrogen, a cytosolic extract was obtained, expression levels of SUCNR1, PGC-1α, transcription factors (NRF1, TFAM), VEGF, catalytic subunits of mitochondrial respiratory enzymes (NDUFV2, SDHA, cyt c1, COX2) and ATP synthases (ATP5A) were determined by Western blot analysis. The study showed that the content of PGC-1α in the peri-infarct zone decreased one day after the induction of ischemic damage by 40% and remained reduced for 21 days after a ischemia. The course of injection of mexidol stabilized PGC-1α in the peri-ischemic zone at a level comparable to the control, both at the stage of treatment and drug withdrawal, and in intact rats induced PGC-1α by 30%. Induction of NRF1, TFAM, NDUFV2, SDHA, cyt c1, ATP5A, indicating the activation of PGC-1α, was observed in rats of the three compared groups, however, the highest expression levels were found in animals subjected to the course of mexidol. Also it was revealed overexpression of SUCNR1 and VEGF in ischemic and intact rats, were injected with mexidol. The study demonstrates for the first time that succinate/SUCNR1 signaling is involved not only in the mechanisms of cerebral angiogenesis, but also in the mechanisms of PGC-1α-dependent neuroprotection. The study opens up new perspectives for pharmacological modulation of PGC-1α levels in the ischemic brain.

scholarly journals Crocetin Isolated from the Natural Food Colorant Saffron Reduces Intracellular Fat in 3T3-L1 Adipocytes

Foods ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1648
Author(s):  
Elena Jiménez-Ortega ◽  
Aitana Braza-Boïls ◽  
Miguel Burgos ◽  
Natalia Moratalla-López ◽  
Manuel Vicente ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Low Cost ◽  
Natural Food ◽  
Peroxisome Proliferator ◽  
Synthetic Dyes ◽  
Potential Candidate ◽  
Peroxisome Proliferator Activated Receptor ◽  
Food Colorant ◽  
Enhancer Binding Protein ◽  
Diphenyltetrazolium Bromide

Saffron, as a food colorant, has been displaced by low-cost synthetic dyes. These have unhealthy properties; thus, their replacement with natural food colorants is an emerging trend. Obesity is a worldwide health problem due to its associated comorbidities. Crocetin esters (crocins) are responsible for the red saffron color. Crocetin (CCT) exhibits healthful properties. We aimed to broaden the existing knowledge on the health properties of CCT isolated from saffron, to facilitate its consideration as a healthy natural food colorant in the future. We evaluated the ability of CCT (1 and 5 μM) to reduce lipid accumulation during the differentiation of 3T3-L1 preadipocytes. Intracellular fat was quantified by Oil Red O staining. CTT cytotoxicity was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The number and size of lipid droplets were analyzed using WimLipid software. The expression of adipogenic genes (CCAAT/enhancer-binding protein (C/EBPβ, C/EBPδ, C/EBPα), and peroxisome proliferator-activated receptor γ (PPARγ)) was analyzed using quantitative real-time PCR (qRT-PCR). CCT 5 μM decreased intracellular fat by 22.6%, without affecting viability or lipid droplet generation, via a decrease in C/EBPα expression, implicated in lipid accumulation. Thus, CCT is a potential candidate to be included in dietary therapies aimed at reversing adipose tissue accumulation in obesity.

scholarly journals Carbamazepine Enhances Adipogenesis by Inhibiting Wnt/β-catenin Expression

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1460 ◽  
Author(s):  
Im ◽  
Kim ◽  
Chau ◽  
Um
Keyword(s):  
Fatty Acid Synthase ◽  
Glycogen Synthase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Negative Regulator ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Expression Levels ◽  
Density Lipoprotein Receptor ◽  
Prevalence Of Obesity

Carbamazepine is a drug that is widely used in the treatment of epilepsy and bipolar disorder. The prevalence of obesity in patients treated with carbamazepine has been frequently reported. However, whether carbamazepine affects adipogenesis, one of the critical steps in the development of obesity, remains unclear. Here, we show that carbamazepine increased the expression levels of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein β (C/EBPβ), and fatty acid synthase (FASN) in 3T3-L1 cells. Notably, carbamazepine inhibited the expression levels of β-catenin, a negative regulator of adipogenesis, leading to enhanced adipogenesis. Conversely, β-catenin overexpression abolished the effect of carbamazepine on adipogenic gene expression. However, depletion of β-catenin further enhanced PPARγ expression. In addition, carbamazepine reduced β-catenin expression by lowering the levels of phospho-low density lipoprotein receptor-related protein 6 (p-LRP6) and phospho-glycogen synthase kinase 3β (p-GSK3β) in Wnt/β-catenin signaling. Moreover, carbamazepine reduced Wnt mRNA expression and decreased the promoter activities of TCF, the target of β-catenin during adipogenesis. These results suggest that carbamazepine enhances adipogenesis by suppressing Wnt/β-catenin expression, indicating its potential effects on obesity-related metabolism.

scholarly journals Pparg may Promote Chemosensitivity of Hypopharyngeal Squamous Cell Carcinoma

PPAR Research ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Meng Lian ◽  
Jiaming Chen ◽  
Xixi Shen ◽  
Lizhen Hou ◽  
Jugao Fang
Keyword(s):  
Gene Expression ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Large Scale ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Regulatory Pathways ◽  
Hypopharyngeal Squamous Cell Carcinoma ◽  
Expression Levels

The upregulation of peroxisome proliferator-activated receptor gamma (PPARG) has been shown to increase the chemosensitivity of several human cancers. This study is aimed at studying if PPARG sensitizes hypopharyngeal squamous cell carcinoma (HSCC) in chemotherapeutic treatments and at dissecting possible mechanisms of observed effects. We integrated large-scale literature data and HSCC gene expression data to identify regulatory pathways that link PPARG and chemosensitivity in HSCC. Expression levels of molecules within the PPARG regulatory pathways were compared in 21 patients that underwent chemotherapy for primary HSCC, including 12 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP). In the CPS group, expression levels of PPARG were higher than that in the CNSP group (log‐fold‐change=0.50). Structured text mining identified two chemosensitivity-related regulatory pathways driven by PPARG. In the CSP group, expression levels for 7 chemosensitivity-promoting genes were increased, while for 13 chemosensitivity suppressing the gene expression levels were decreased. Our results support the chemosensitivity-promoting role of PPARG in HSCC tumor cells, most likely by affecting both cell proliferation and cell motility pathways.

scholarly journals Changes in adipose tissue physiology during the first two weeks posthatch in chicks from lines selected for low or high body weight

2019 ◽  
Vol 316 (6) ◽  
pp. R802-R818 ◽  
Author(s):  
Yang Xiao ◽  
Guoqing Wang ◽  
Miranda E. Gerrard ◽  
Sarah Wieland ◽  
Mary Davis ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Fat Mass ◽  
Peroxisome Proliferator ◽  
Adipocyte Size ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nonesterified Fatty Acids ◽  
Development Patterns ◽  
Fat Depots ◽  
Enhancer Binding Protein

Chickens from lines selected for low (LWS) or high (HWS) body weight (BW) differ in appetite and adiposity. Mechanisms associated with the predisposition to becoming obese are unclear. The objective of the experiment was to evaluate developmental changes in depot-specific adipose tissue during the first 2 wk posthatch. Subcutaneous (SQ), clavicular (CL), and abdominal (AB) depots were collected at hatch (DOH) and days 4 (D4) and 14 (D14) posthatch for histological and mRNA measurements. LWS chicks had decreased SQ fat mass on a BW basis with reduced adipocyte size from DOH to D4 and increased BW and fat mass with unchanged adipocyte size from D4 to D14. HWS chicks increased in BW from DOH to D14 and increased in fat mass in all three depots with enlarged adipocytes in the AB depot from D4 to D14. Meanwhile, CCAAT/enhancer-binding protein-α, neuropeptide Y, peroxisome proliferator-activated receptor-γ, and acyl-CoA dehydrogenase mRNAs differed among depots between lines at different ages. Plasma nonesterified fatty acids were greater in LWS than HWS at D4 and D14. From DOH to D4, LWS chicks mobilized SQ fat and replenished the reservoir through hyperplasia, whereas HWS chicks were dependent on hyperplasia and hypertrophy to maintain adipocyte size and depot mass. From D4 to D14, adipose tissue catabolism and adipogenesis slowed. Whereas LWS fat depots and adipocyte sizes remained stable, HWS chicks rapidly accumulated fat in CL and AB depots. Chicks predisposed to be anorexic or obese have different fat development patterns during the first 2 wk posthatch.

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