FOOD SECURITY: EFFECT ON PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA (PPARY) AND BMI AMONG YOUNG ADULT

2016 ◽  
Vol 78 (6-8) ◽  
Author(s):  
Nur Atiqah Alias ◽  
Norazmir Md Nor ◽  
Mohd Fahmi Mastuki ◽  
Khairil Anuar Md Isa
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Food Security ◽  
Adipocyte Differentiation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Food Security Status ◽  
Metabolic Indices ◽  
Pparγ Expression ◽  
Sensitivity Increase

Food security status is a method used to differentiate food secure and food insecure experience. Throughout our lives, nutritious food and lifestyle are closely related with most lifestyle-associated illness. This study investigated young adults in both groups to determine molecular changes on gene expression of peroxisome proliferator-activated receptor-gamma (PPARγ). PPARγ plays an important role in adipocyte differentiation, fatty acids, and insulin sensitivity. Increase of PPARγ expression help to improve metabolic indices in dysregulated metabolism associated with obesity, diabetes, and cardiovascular disease. There are no significant differences (P>0.05) of PPARγ expression and BMI for both groups. However, expression of PPARγ is detected in earlier amplification for food insecure group. Mean of BMI (20.70± 3.025) is also slightly higher in food insecure group than food secure. Conclusively, there are some effects on expression of PPARγ and BMI based on food security status. 

scholarly journals Increasing Fat Deposition via Upregulates the Transcription of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) in Native Crossbred Chicken

2020 ◽  
Author(s):  
Supanon Tunim ◽  
Yupin Phasuk ◽  
Samuel E. Aggrey ◽  
Monchai Duangjinda
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Intramuscular Fat ◽  
Abdominal Fat ◽  
Fat Deposition ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Chicken Breeds ◽  
Pparγ Expression ◽  
Pparγ Gene

Abstract Background: Crossbreeding using exotic breeds is usually employed to improve the growth characteristics of indigenous chickens. This mating not only provides growth but affect adversely to fat deposition as well. We studied the growth, abdominal, subcutaneous and intramuscular fat and mRNA expression of peroxisome proliferator-activated receptor (PPAR) α and PPARγ in adipose and muscle tissues of four chicken breeds [Chee breed (CH) (100% Thai native chicken), Kaimook e-san1 (KM1; 50% CH background), Kaimook e-san2 (KM2; 25% CH background), and broiler (BR)]. This study was aim to study role of PPARs on fat deposition in native crossbred chicken.Results: The BR chickens had higher abdominal fat than other breeds (P<0.05) and the KM2 had an abdominal fat percentage higher than KM1 and CH respectively (P<0.05). The intramuscular fat (IMF) of BR was greater than KM1 and CH (P<0.05). In adipose tissue, PPARα transcription expression was different among the chicken breeds. However, there were breed differences in PPARγ gene expression. Study of abdominal fat PPARγ gene expression showed the BR breed, KM1, and KM2 breed significantly greater (P<0.05) than CH. In 8 to 12 weeks of age, the result shows that the PPARγ expression of the CH breed is less than (P<0.05) KM2. The result of PPARs expression in muscle tissue was similar result in adipose tissue.Conclusion: Crossbreeding improved the growth of the Thai native breed, there was also a corresponding increase in carcass fatness. However, there appears to be a relationship between PPARγ expression and fat deposition traits. therefore, PPARγ activity plays a key role in lipid accumulation by up-regulation.

scholarly journals Activated Liver X Receptors Stimulate Adipocyte Differentiation through Induction of Peroxisome Proliferator-Activated Receptor γ Expression

2004 ◽  
Vol 24 (8) ◽  
pp. 3430-3444 ◽  
Author(s):  
Jong Bae Seo ◽  
Hyang Mi Moon ◽  
Woo Sik Kim ◽  
Yun Sok Lee ◽  
Hyun Woo Jeong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Target Gene ◽  
Adipocyte Differentiation ◽  
Specific Gene ◽  
Peroxisome Proliferator ◽  
Liver X Receptors ◽  
Gene Promoters ◽  
Peroxisome Proliferator Activated Receptor ◽  
Specific Gene Expression ◽  
X Receptors

ABSTRACT Liver X receptors (LXRs) are nuclear hormone receptors that regulate cholesterol and fatty acid metabolism in liver tissue and in macrophages. Although LXR activation enhances lipogenesis, it is not well understood whether LXRs are involved in adipocyte differentiation. Here, we show that LXR activation stimulated the execution of adipogenesis, as determined by lipid droplet accumulation and adipocyte-specific gene expression in vivo and in vitro. In adipocytes, LXR activation with T0901317 primarily enhanced the expression of lipogenic genes such as the ADD1/SREBP1c and FAS genes and substantially increased the expression of the adipocyte-specific genes encoding PPARγ (peroxisome proliferator-activated receptor γ) and aP2. Administration of the LXR agonist T0901317 to lean mice promoted the expression of most lipogenic and adipogenic genes in fat and liver tissues. It is of interest that the PPARγ gene is a novel target gene of LXR, since the PPARγ promoter contains the conserved binding site of LXR and was transactivated by the expression of LXRα. Moreover, activated LXRα exhibited an increase of DNA binding to its target gene promoters, such as ADD1/SREBP1c and PPARγ, which appeared to be closely associated with hyperacetylation of histone H3 in the promoter regions of those genes. Furthermore, the suppression of LXRα by small interfering RNA attenuated adipocyte differentiation. Taken together, these results suggest that LXR plays a role in the execution of adipocyte differentiation by regulation of lipogenesis and adipocyte-specific gene expression.

Regulation of adipocyte differentiation of 3T3-L1 cells by PDZRN3

2013 ◽  
Vol 304 (11) ◽  
pp. C1091-C1097 ◽  
Author(s):  
Takeshi Honda ◽  
Aiko Ishii ◽  
Makoto Inui
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Adipogenic Differentiation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Protein Levels ◽  
Upstream Regulator ◽  
Pparγ Expression

PDZRN3, a member of the PDZRN (or LNX) family of proteins, is essential for the differentiation of mesenchymal stem cells into myotubes, but it plays an inhibitory role in the differentiation of these cells into osteoblasts. Given that mesenchymal stem cells also differentiate into adipocytes, we examined the possible role of PDZRN3 in adipogenesis in mouse 3T3-L1 preadipocytes. The expression of PDZRN3 decreased at both the mRNA and protein levels during adipogenic differentiation. RNAi-mediated depletion of PDZRN3 enhanced the differentiation of 3T3-L1 cells into adipocytes as assessed on the basis of lipid accumulation. The upregulation of aP2 and CCAAT/enhancer-binding protein (C/EBP)-β during adipocyte differentiation was also enhanced in the PDZRN3-depleted cells, as was the induction of peroxisome proliferator-activated receptor-γ (PPARγ), an upstream regulator of aP2 and C/EBPα, at both the mRNA and protein levels. Among transcription factors that control the expression of PPARγ, we found that STAT5b, but not STAT5a, was upregulated in PDZRN3-depleted cells at both mRNA and protein levels. Tyrosine phosphorylation of STAT5b, but not that of STAT5a, was also enhanced at an early stage of differentiation by PDZRN3 depletion. In addition, the expression of C/EBPβ during the induction of differentiation was enhanced at the mRNA and protein levels in PDZRN3-depleted cells. Our results thus suggest that PDZRN3 negatively regulates adipogenesis in 3T3-L1 cells through downregulation of STAT5b and C/EBPβ and consequent suppression of PPARγ expression.

scholarly journals Peroxisome-proliferator-activated receptor γ suppresses Wnt/β-catenin signalling during adipogenesis

2003 ◽  
Vol 376 (3) ◽  
pp. 607-613 ◽  
Author(s):  
Marthe MOLDES ◽  
Ying ZUO ◽  
Ron F. MORRISON ◽  
David SILVA ◽  
Bae-Hang PARK ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Ectopic Expression ◽  
Reciprocal Relationship ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Activation Of Transcription ◽  
Undifferentiated State ◽  
Ectopic Production ◽  
Pparγ Expression

The Wnt/β-catenin signalling pathway appears to operate to maintain the undifferentiated state of preadipocytes by inhibiting adipogenic gene expression. To define the mechanisms regulating suppression of Wnt/β-catenin signalling, we analysed the β-catenin expression in response to activation of transcription factors that regulate adipogenesis. The results show an extensive down-regulation of nuclear β-catenin that occurs during the first few days of differentiation of 3T3-L1 preadipocytes and coincides with the induction of the adipogenic transcription factors, C/EBPβ (CCAAT-enhancer-binding protein) and PPARγ (peroxisome-proliferator-activated receptor). To assess the role of each of these factors in this process, we conditionally overexpressed C/EBPβ in Swiss mouse fibroblasts using the TET-off system. Abundant expression of C/EBPβ alone had minimal effect on β-catenin expression, whereas expression of C/EBPβ, in the presence of dexamethasone, induced PPARγ expression and caused a measurable decrease in β-catenin. In addition, exposure of cells expressing both C/EBPβ and PPARγ to a potent PPARγ ligand resulted in an even greater decrease in β-catenin by mechanisms that involve the proteasome. Our studies also suggest a reciprocal relationship between PPARγ activity and β-catenin expression, since ectopic production of Wnt-1 in preadipocytes blocked the induction of PPARγ gene expression. Moreover, by suppressing β-catenin expression, ectopic expression of PPARγ in Wnt-1-expressing preadipocytes rescued the block in adipogenesis after their exposure to the PPARγ ligand, troglitazone.

scholarly journals Decreased Expression of Peroxisome Proliferator-activated Receptor α Gene as an Indicator of Metabolic Disorders in Stunting Toddler

2020 ◽  
Vol 8 (A) ◽  
pp. 175-180
Author(s):  
Khairun Nisa Berawi ◽  
Ani Melani Maskoen ◽  
Leva Akbar
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Mrna Expression ◽  
Metabolic Disorders ◽  
Metabolic Changes ◽  
Trigger Factor ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Mrna Gene ◽  
Gene Mrna

BACKGROUND: Stunting in children increases the risk of degenerative diseases in adulthood, including dyslipidemia, obesity, type 2 diabetes mellitus, and cardiovascular disease. This is based on the result of metabolic changes that may be caused by chronic malnutrition and experienced by stunting children. Stunting in children is associated with metabolic disorders that are based on impaired fat oxidation, a trigger factor for obesity in adulthood. The peroxisome proliferator-activated receptor (PPAR) α gene is a transcriptional factor that regulates fat, carbohydrate, and amino acid metabolism whose genetic variants are linked to the development of dyslipidemia and cardiovascular disease. AIM: The study assessed the effect of metabolic changes in stunting toddler on PPARα gene expression. MATERIALS AND METHODS: An analytical-observational laboratory was done using 41 blood samples, coming from 23 stunting toddlers, and 18 not-stunting toddlers. In all research subjects, anthropometric measurements and examination of PPARα gene mRNA expression were carried out. Analysis of PPARα gene mRNA expression using one-step quantitative reverse transcriptase-polymerase chain reaction using specific primers, as a comparison of gene expression using the GAPDH gene. The relative expression of the PPARα mRNA gene was analyzed using the LIVAK formula. RESULTS: The study obtained a mean of ΔCT in stunting toddlers of 5.81, whereas in stunting toddlers at 5.082. Analysis with LIVAK 2 ^ - formula (ΔCT stunting -ΔCT not stunting) obtained PPARα mRNA gene expression of 0.6. CONCLUSION: We conclude that there is a decrease in PPARα gene expression in stunting toddlers.

scholarly journals Transcription Suppression of Peroxisome Proliferator-Activated Receptor γ2 Gene Expression by Tumor Necrosis Factor α via an Inhibition of CCAAT/ Enhancer-binding Protein δ during the Early Stage of Adipocyte Differentiation

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4948-4956 ◽  
Author(s):  
Masataka Kudo ◽  
Akira Sugawara ◽  
Akira Uruno ◽  
Kazuhisa Takeuchi ◽  
Sadayoshi Ito
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Gene Transcription ◽  
Adipocyte Differentiation ◽  
Early Stage ◽  
Binding Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Protein Levels ◽  
Enhancer Binding Protein

Abstract TNFα is known to inhibit adipocyte differentiation and induce insulin resistance. Moreover, TNFα is known to down-regulate peroxisome proliferator-activated receptor (PPAR)γ2, an adipocyte-specific nuclear receptor of insulin-sensitizer thiazolidinediones. To clarify molecular mechanisms of TNFα- mediated PPARγ2 down-regulation, we here examined the effect of TNFα on transcription regulation of PPARγ2 gene expression during the early stage of adipocyte differentiation. 3T3-L1 preadipocytes (2 d after 100% confluent) were incubated in a differentiation mixture (dexamethasone, insulin, 3-isobutyl-1-methlxanthine), with or without 50 ng/ml TNFα, for 24 h. TNFα significantly decreased PPARγ2 expression both at mRNA and protein levels (to ∼40%), as well as aP2 mRNA expression. The mouse PPARγ2 gene promoter region (2.2-kb) was isolated and was used for luciferase reporter assays by transient transfection. TNFα significantly suppressed PPARγ2 gene transcription (to ∼50%), and deletion analyses demonstrated that the suppression was mediated via CCAAT/enhancer-binding protein (C/EBP) binding elements at the −320/−340 region of the promoter. Moreover, TNFα significantly decreased expression of C/EBPδ mRNA and protein levels (to ∼40%). EMSA, using 3T3-L1 cells nuclear extracts with the −320/−340 region as a probe, demonstrated the binding of C/EBPδ to the element, which was significantly decreased by TNFα treatment. Overexpression of CEBP/δ prevented the TNFα-mediated suppression of PPARγ2 transactivation. Taken together, TNFα suppresses PPARγ2 gene transcription by the inhibition of C/EBPδ expression and its DNA binding during the early stage of adipocyte differentiation, which may contribute to the inhibition of adipocyte differentiation, as well as the induction of insulin resistance.

scholarly journals Shockwaves Suppress Adipocyte Differentiation via Decrease in PPARγ

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 166
Author(s):  
Wonkyoung Cho ◽  
SeoYeon Kim ◽  
Myeongsook Jeong ◽  
Young Mi Park
Keyword(s):  
Adipocyte Differentiation ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Intracellular Camp ◽  
Peroxisome Proliferator ◽  
Mechanical Stimuli ◽  
Western Blots ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pparγ Expression ◽  
Camp Levels

Adipogenesis is a crucial cellular process that contributes to the expansion of adipose tissue in obesity. Shockwaves are mechanical stimuli that transmit signals to cause biological responses. The purpose of this study is to evaluate the effects of shockwaves on adipogenesis. We treated 3T3L-1 cells and human primary preadipocytes for differentiation with or without shockwaves. Western blots and quantitative real-time reverse transcriptase PCR (qRT-PCR) for adipocyte markers including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding proteins (C/EBPα) were performed. Extracellular adenosine triphosphate (ATP) and intracellular cyclic adenosine monophosphate (cAMP) levels, which are known to affect adipocyte differentiation, were measured. Shockwave treatment decreased intracellular lipid droplet accumulation in primary human preadipocytes and 3T3-L1 cells after 11–12 days of differentiation. Levels of key adipogenic transcriptional factors PPARγ and/or C/EBPα were lower in shockwave-treated human primary preadipocytes and 3T3L-1 cells after 12–13 days of differentiation than in shockwave-untreated cells. Shockwave treatment induced release of extracellular ATP from preadipocytes and decreased intracellular cAMP levels. Shockwave-treated preadipocytes showed a higher level of β-catenin and less PPARγ expression than shockwave-untreated cells. Supplementation with 8-bromo-cAMP analog after shockwave treatment rescued adipocyte differentiation by preventing the effect of shockwaves on β-catenin, Wnt10b mRNA, and PPARγ expression. Low-energy shockwaves suppressed adipocyte differentiation by decreasing PPARγ. Our study suggests an insight into potential uses of shockwave-treatment for obesity.

Transcriptional regulation of the human acetoacetyl-CoA synthetase gene by PPARγ

2010 ◽  
Vol 427 (2) ◽  
pp. 255-264 ◽  
Author(s):  
Francesca Aguiló ◽  
Nuria Camarero ◽  
Joana Relat ◽  
Pedro F. Marrero ◽  
Diego Haro
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Target Gene ◽  
Adipocyte Differentiation ◽  
Ketone Bodies ◽  
Physiological Role ◽  
Direct Interaction ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Human Promoter

In the cytosol of lipogenic tissue, ketone bodies are activated by AACS (acetoacetyl-CoA synthetase) and incorporated into cholesterol and fatty acids. AACS gene expression is particularly abundant in white adipose tissue, as it is induced during adipocyte differentiation. In order to elucidate the mechanism controlling the gene expression of human AACS and to clarify its physiological role, we isolated the human promoter, characterized the elements required to initiate transcription and analysed the expression of the gene in response to PPARγ (peroxisome-proliferator-activated receptor γ), an inducer of adipogenesis. We show that the human AACS promoter is a PPARγ target gene and that this nuclear receptor is recruited to the AACS promoter by direct interaction with Sp1 (stimulating protein-1).

scholarly journals EFFECT OF TROGLITAZONE ON MORPHOLOGICAL CHANGES AND PPAR-γ GENE EXPRESSION IN 3T3-L1 ADIPOCYTE CELLS

2019 ◽  
Vol 6 (1) ◽  
pp. 53
Author(s):  
Asri Sulfianti ◽  
Mayriska Triwulansari ◽  
. Nuralih ◽  
. Churiyah
Keyword(s):  
Gene Expression ◽  
Adipocyte Differentiation ◽  
Morphological Changes ◽  
Mrna Level ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hypoglycemic Agent ◽  
Ppar Γ ◽  
Oil Red O Staining ◽  
Oil Red O

Efek Troglitazone terhadap Perubahan Morfologi dan Ekspresi Gen PPAR- γ di Dalam Sel Adiposa 3T3-L1 ABSTRACT3T3-L1 cells are extensively used as a model to study adipogenesis. However, one major concern is the prolonged period of time it takes the cells to differentiate into adipocytes form. To induce this differentiation, the adipogenic induction media is required. In this study, troglitazone, a hypoglycemic agent was added to adipogenic induction media and observed in order to determine the morphological changes and peroxisome proliferator-activated receptor gamma (PPAR-γ) gene expression in 3T3-L1 differentiation. It is generally known that PPAR-ꝩ plays an important role as a transcription factor in adipocyte differentiation. Based on Oil Red O Staining, adipogenic induction with or without troglitazone changed the 3T3-L1 pre-adipocytes into mature round fat cells characterized by red droplet lipids. This cell also had a high absorbance level and degree of droplet accumulation of P≤ 0.05 in each group. In addition, cells treated by troglitazone had the highest PPAR-ꝩ mRNA level (1.9 fold) than those treated by adipogenic induction media without troglitazone or cells un-treated at all. Keywords: 3T3-L1, adipocyte, differentiation, PPAR-ꝩ, troglitazone ABSTRAKSel 3T3-L1 adalah jenis sel yang banyak digunakan dalam studi adipogenesis. Namun, salah satu kelemahan sel tersebut adalah lamanya waktu yang dibutuhkan bagi sel pre-adiposa untuk berdiferensiasi menjadi sel adiposa. Selain itu, dibutuhkan pula media induksi khusus untuk mengubah sel menjadi sel adiposa. Pada penelitian ini, kami mengobservasi fungsi troglitazone, sebagai antidiabetes terhadap perubahan morfologi dan ekspresi gen peroxisome proliferator-activated receptor gamma (PPAR-γ). Telah diketahui bahwa PPAR-ꝩ berperan penting sebagai factor transkripsi dalam diferensasi sel adiposa. Berdasarkan pewarnaan ORO, induksi sel pre-adiposa 3T3-L1 dengan media induksi dengan dan tanpa troglitazone merubah sel preadiposa menjadi sel berbentuk bulat yang dikarakterisasi dengan akumulasi droplet lemak. Nilai absorbansi sel adiposa juga menandakan adanya perbedaan yang signifikan antara kelompok sel yang diberi troglitazone dan tidak, dan sel tanpa diberi media induksi. Sementara, pada kelompok sel yang diberi troglitazone memiliki ekspresi mRNA PPAR-ꝩ (1,9 kali) tertinggi jika dibandingkan dengan sel yang diberi media induksi tanpa troglitazone, dan tanpa media induksi sama sekali.Kata Kunci: 3T3-L1, adiposa, diferensiasi, PPAR-ꝩ, troglitazone

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