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.

scholarly journals Anti-Allergic and Anti-Inflammatory Effects of Undecane on Mast Cells and Keratinocytes

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1554
Author(s):  
Dabin Choi ◽  
Wesuk Kang ◽  
Taesun Park
Keyword(s):  
Mast Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Allergic Diseases ◽  
Intracellular Camp ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Skin Conditions ◽  
Factor Α ◽  
Camp Levels

The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.

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.

Genetic Polymorphisms of the ß2-Adrenergic Receptor Relate to Guanosine Protein-coupled Stimulator Receptor Dysfunction in Fibromyalgia Syndrome

2011 ◽  
Vol 38 (6) ◽  
pp. 1095-1103 ◽  
Author(s):  
YANGMING XIAO ◽  
WEIJING HE ◽  
I. JON RUSSELL
Keyword(s):  
Adrenergic Receptor ◽  
Fibromyalgia Syndrome ◽  
Mononuclear Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Intracellular Camp ◽  
Peripheral Blood Mononuclear ◽  
Genotype Frequencies ◽  
Camp Levels

Objective.To determine the genotype frequencies of ß2-adrenergic receptor (ß2AR) gene polymorphisms (Gly16Arg, Glu27Gln) in patients with fibromyalgia syndrome (FM) by comparison with unrelated healthy controls. We sought any clinical association with these polymorphisms and determined whether the polymorphisms would associate with a biologic guanosine protein-coupled stimulator receptor (Gs) dysfunction in FM.Methods.Study subjects included 97 clinically characterized patients with FM and 59 controls. The ß2AR polymorphisms at codons 16 and 27 were determined using polymerase chain reaction-restriction fragment length polymorphism. The Gs functions of peripheral blood mononuclear cells (PBMC) were tested using isoproterenol (ISO) as the adrenergic Gs ligand and measuring intracellular cyclic adenosine monophosphate (cAMP) levels.Results.The frequency of the ß2AR gene polymorphism Gly16Arg in FM (43.5%) was significantly lower than in controls (63.2%), suggesting that this genotype might have some effect on the risk of developing FM. The only clinical association in FM was with sleep dysfunction. Patients with FM who carried the ß2AR polymorphism Arg16Arg also exhibited significantly lower PBMC basal cAMP levels (p < 0.05) and lower ISO-stimulated cAMP levels (p < 0.05) than FM carrying Gly16Gly or Gly16Arg.Conclusion.This confirms a relationship between ß2AR polymorphism and FM. It is the first study to demonstrate ß2AR polymorphism-related differences in intracellular cAMP responses of FM PBMC after ß2AR stimulationin vitro. These findings may explain some of the differences in responsiveness of FM subgroups to the adrenergic agonist medications currently approved for FM treatment.

scholarly journals . Effect of fluoxetine on the inhibition of adenylate cyclase activity in foskolin-stimulated MLTC-1 leydig cells

2020 ◽  
Vol 17 (4) ◽  
pp. 595-602
Author(s):  
Nguyen Thi Mong Diep ◽  
Nguyen Thi Bich Hang ◽  
Nguyen Le Cong Minh ◽  
Tran Thanh Son ◽  
Nguyen Thuy Duong
Keyword(s):  
Cyclic Amp ◽  
Leydig Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Cell Types ◽  
Intracellular Camp ◽  
Atp Levels ◽  
Long Time ◽  
Short Time ◽  
Camp Levels

Fluoxetine (FLX), a widely used antidepressant primarily acting as a selective serotonin reuptake inhibitor, has been shown to exhibit other mechanisms of action in various cell types. Cyclic adenosine monophosphate (cAMP) is a second messenger used for intracellular signal induction. Cyclic AMP is a nucleotide synthesized within the cell from adenosine triphosphate by the adenylyl cyclase enzyme, and is inactivated enzymatically to 5′AMP by hydroxylation with a group of enzymes called phosphodiesterase. The aim of this study was to determine the effects of FLX on MLTC-1 Leydig cells on intracellular cyclic AMP response to forskolin (FSK). MLTC-1 cells were incubated at 37°C in media supplemented with or without different doses of FLX (0, 0.156, 0.3125, 0.625, 1.25, 2.5, 5 and 10 µM). We then looked for how the concentration of FLX for a short-time (2 hours) and a long-time (24 hours) affects the concentration of intracellular cyclic AMP response to FSK and ATP levels on MLTC-1 cells. Our results show that FLX decreased the intracellular cAMP response to FSK depending on FLX concentration. FLX decreased significantly cAMP levels only at 10 µM after 2 hours of incubation but after 24 hours of incubation FLX caused an effect on cAMP levels at 5 µM and at 10 µM. Moreover, as expected, FLX also caused a decline of steroidogenesis, which is under the control of cAMP and ATP levels in the cells. Taken together, these findings demonstrate that the inhibition of cAMP synthesis by FLX is dose-dependent, and that FLX also inhibited hormone-induced steroidogenesis in MLTC-1 cells.

scholarly journals Flavonoids from Acer okamotoanum Inhibit Adipocyte Differentiation and Promote Lipolysis in the 3T3-L1 Cells

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1920 ◽  
Author(s):  
Ji Hyun Kim ◽  
Sanghyun Lee ◽  
Eun Ju Cho
Keyword(s):  
Fatty Acid Synthase ◽  
Glucose Transporter ◽  
Adipocyte Differentiation ◽  
Adenosine Monophosphate ◽  
Hormone Sensitive Lipase ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Acer Okamotoanum ◽  
Related Proteins

Flavonoids, quercitrin, isoquercitrin (IQ), and afzelin, were isolated from ethyl acetate fraction of Acer okamotoanum. We investigated anti-obesity effects and mechanisms of three flavonoids from A. okamotoanum in the differentiated 3T3-L1 cells. The differentiated 3T3-L1 cells increased triglyceride (TG) contents, compared with non-differentiated normal group. However, treatments of three flavonoids from A. okamotoanum decreased TG contents without cytotoxicity. In addition, they showed significant down-regulation of several adipogenic transcription factors, such as γ-cytidine-cytidine-adenosine-adenosine-thymidine/enhancer binding protein -α, -β, and peroxisome proliferator-activated receptor-γ, compared with non-treated control group. Furthermore, treatment of the flavonoids inhibited expressions of lipogenesis-related proteins including fatty acid synthase, adipocyte protein 2, and glucose transporter 4. Moreover, IQ-treated group showed significant up-regulation of lipolysis-related proteins such as adipose triglyceride lipase and hormone-sensitive lipase. In addition, flavonoids significantly activated 5′-adenosine monophosphate-activated protein kinase (AMPK) compared to control group. In particular, IQ showed higher inhibition of TG accumulation by regulation of pathways related with both adipogenesis and lipolysis, than other flavonoids. The present results indicated that three flavonoids of A. okamotoanum showed anti-obesity activity by regulation of adipocyte differentiation, lipolysis, and AMPK signaling, suggesting as an anti-obesity functional agents.

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 Regulation of Peroxisome Proliferator-Activated Receptor γ Expression by Adipocyte Differentiation and Determination Factor 1/Sterol Regulatory Element Binding Protein 1: Implications for Adipocyte Differentiation and Metabolism

1999 ◽  
Vol 19 (8) ◽  
pp. 5495-5503 ◽  
Author(s):  
Lluis Fajas ◽  
Kristina Schoonjans ◽  
Laurent Gelman ◽  
Jae B. Kim ◽  
Jamila Najib ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Pparγ Expression

ABSTRACT Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor implicated in adipocyte differentiation and insulin sensitivity. We investigated whether PPARγ expression is dependent on the activity of adipocyte differentiation and determination factor 1/sterol regulatory element binding protein 1 (ADD-1/SREBP-1), another transcription factor associated with both adipocyte differentiation and cholesterol homeostasis. Ectopic expression of ADD-1/SREBP-1 in 3T3-L1 and HepG2 cells induced endogenous PPARγ mRNA levels. The related transcription factor SREBP-2 likewise induced PPARγ expression. In addition, cholesterol depletion, a condition known to result in proteolytic activation of transcription factors of the SREBP family, induced PPARγ expression and improved PPRE-driven transcription. The effect of the SREBPs on PPARγ expression was mediated through the PPARγ1 and -3 promoters. Both promoters contain a consensus E-box motif that mediates the regulation of the PPARγ gene by ADD-1/SREBP-1 and SREBP-2. These results suggest that PPARγ expression can be controlled by the SREBP family of transcription factors and demonstrate new interactions between transcription factors that can regulate different pathways of lipid metabolism.

scholarly journals Hypothalamic orexin A expression and the involvement of AMPK and PPAR-gamma signalling in energy restricted dairy cows

2011 ◽  
Vol 54 (6) ◽  
pp. 567-579 ◽  
Author(s):  
B. Kuhla ◽  
S. Görs ◽  
C. C. Metges
Keyword(s):  
Dairy Cows ◽  
Adenosine Monophosphate ◽  
Ppar Gamma ◽  
Energy Restriction ◽  
Plasma Metabolites ◽  
Peroxisome Proliferator ◽  
Orexin A ◽  
Hypothalamic Area ◽  
Western Blots ◽  
Peroxisome Proliferator Activated Receptor

Abstract. A number of circuits controlling feed intake have been identified in rodents in which circulating dietary metabolites are detected by the brainstem and the hypothalamus converting these input signals to anorexic responses. Dietary metabolites used by dairy cows, however, are not identical with those of rodents calling for the elucidation of feedingrelated pathways in ruminants. In the present study we examined potentially relevant plasma metabolites and hypothalamic signalling pathways in ad libitum and restrictively fed early lactating dairy cows. 60 h feed energy restriction led to significantly increased non-esterified fatty acid (NEFA), Gln, Gly, His, and 3-Me-histine but decreased Asp, Asn, beta-Ala, Tyr, and Trp concentrations. In immunohistochemical studies, we found that feed energy restriction is associated with elevated numbers of parvocellular but not magnocellular orexin A neurons in the lateral, dorsomedial and posterior hypothalamic area. In parvocellular orexin A neurons we determined complete colocalisation with cFOS in energy restricted cows. In the majority of orexin A neurons we further found colocalisation with activated adenosine monophosphate activated kinase (AMPK) as well as with peroxisome proliferator-activated receptor-gamma (PPARγ). Feed restriction also induced activation (phosphorylation) of AMPK and increased expression of PPARγ when Western Blots were normalized to β-actin. These results suggest that orexin A associated with AMPK and PPARγ signalling is involved in the control of energy homeostasis of dairy cows.

scholarly journals Caffeine in the Treatment of Atopic Dermatitis and Psoriasis: A Review

2019 ◽  
Vol 3 (2) ◽  
pp. 59-71 ◽  
Author(s):  
Mais Bassam Alashqar
Keyword(s):  
Atopic Dermatitis ◽  
Skin Diseases ◽  
Kinase Inhibitor ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Intracellular Camp ◽  
Ataxia Telangiectasia Mutated ◽  
Inflammatory Skin Diseases ◽  
Camp Levels ◽  
Effective Adjunct

   Atopic dermatitis (AD) and psoriasis are inflammatory skin diseases. AD is characterized by immune dysregulation and barrier impairment, while psoriasis is by immune dysfunction and resultant keratinocyte hyper-proliferation.    Caffeine has shown effective in ameliorating the symptoms of both diseases, but it is not conclusive through which pathways. The aim of this study was to provide a detailed discussion of available work on this topic, as well as known modes of action of caffeine that are relevant to these two conditions.    After an extensive review of the literature, we found that both diseases have decreased intracellular cyclic adenosine monophosphate (cAMP) levels in cutaneous leukocytes, so it is very likely that being a methylxanthine, and hence a phosphodiesterase (PDE) inhibitor, caffeine raises intracellular cAMP levels, which suppresses inflammatory pathways and potentiates anti-inflammatory ones. Moreover, caffeine is known to be an ATR (ataxia-telangiectasia mutated) kinase and an ATM (ATM- and Rad3-Related) kinase inhibitor, which promotes prompt apoptosis of damaged cells. It was also found to have anti-necrotic effects in reactive oxygen species (ROS)-damaged cells. These pro-apoptotic and anti-necrotic properties may also be reducing the inflammation. Finally, caffeine's metabolites have shown antioxidising effects against ROS, which certainly would reduce inflammation caused by lipid peroxidation, DNA damage and organelle destruction.    We find that caffeine acts in a number of ways to improve symptoms of inflammation and that it is an effective adjunct to therapy in AD and psoriasis.

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