scholarly journals Polymerase I and transcript release factor (PTRF) regulates adipocyte differentiation and determines adipose tissue expandability

2014 ◽  
Vol 28 (8) ◽  
pp. 3769-3779 ◽  
Author(s):  
Sergio Perez‐Diaz ◽  
Lance A. Johnson ◽  
Robert M. DeKroon ◽  
Jose M. Moreno‐Navarrete ◽  
Oscar Alzate ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Release Factor ◽  
Polymerase I ◽  
Adipose Tissue Expandability

scholarly journals Polymerase I and Transcript Release Factor Regulates Lipolysis via a Phosphorylation-Dependent Mechanism

Diabetes ◽  
2011 ◽  
Vol 60 (3) ◽  
pp. 757-765 ◽  
Author(s):  
Nabila Aboulaich ◽  
Patricia C. Chui ◽  
John M. Asara ◽  
Jeffrey S. Flier ◽  
Eleftheria Maratos-Flier
Keyword(s):  
Release Factor ◽  
Polymerase I ◽  
Dependent Mechanism

scholarly journals Evidence for the Regulatory Role of Lipocalin 2 in High-Fat Diet-Induced Adipose Tissue Remodeling in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3525-3538 ◽  
Author(s):  
Hong Guo ◽  
Merlijn Bazuine ◽  
Daozhong Jin ◽  
Merry M. Huang ◽  
Samuel W. Cushman ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Tissue Remodeling ◽  
Peroxisome Proliferator ◽  
Lipocalin 2 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Adipose Tissue Remodeling ◽  
Fat Depot

Lipocalin 2 (Lcn2) has previously been characterized as an adipokine/cytokine playing a role in glucose and lipid homeostasis. In this study, we investigate the role of Lcn2 in adipose tissue remodeling during high-fat diet (HFD)-induced obesity. We find that Lcn2 protein is highly abundant selectively in inguinal adipose tissue. During 16 weeks of HFD feeding, the inguinal fat depot expanded continuously, whereas the expansion of the epididymal fat depot was reduced in both wild-type (WT) and Lcn2−/− mice. Interestingly, the depot-specific effect of HFD on fat mass was exacerbated and appeared more pronounced and faster in Lcn2−/− mice than in WT mice. In Lcn2−/− mice, adipocyte hypertrophy in both inguinal and epididymal adipose tissue was more profoundly induced by age and HFD when compared with WT mice. The expression of peroxisome proliferator-activated receptor-γ protein was significantly down-regulated, whereas the gene expression of extracellular matrix proteins was up-regulated selectively in epididymal adipocytes of Lcn2−/− mice. Consistent with these observations, collagen deposition was selectively higher in the epididymal, but not in the inguinal adipose depot of Lcn2−/− mice. Administration of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone (Rosi) restored adipogenic gene expression. However, Lcn2 deficiency did not alter the responsiveness of adipose tissue to Rosi effects on the extracellular matrix expression. Rosi treatment led to the further enlargement of adipocytes with improved metabolic activity in Lcn2−/− mice, which may be associated with a more pronounced effect of Rosi treatment in reducing TGF-β in Lcn2−/− adipose tissue. Consistent with these in vivo observations, Lcn2 deficiency reduces the adipocyte differentiation capacity of stromal-vascular cells isolated from HFD-fed mice in these cells. Herein Rosi treatment was again able to stimulate adipocyte differentiation to a similar extent in WT and Lcn2−/− inguinal and epididymal stromal-vascular cells. Thus, combined, our data indicate that Lcn2 has a depot-specific role in HFD-induced adipose tissue remodeling.

Adipocyte differentiation of multipotent cells established from human adipose tissue

2004 ◽  
Vol 315 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Anne-Marie Rodriguez ◽  
Christian Elabd ◽  
Frédéric Delteil ◽  
Julien Astier ◽  
Cécile Vernochet ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Human Adipose Tissue ◽  
Multipotent Cells

Urokinase-type plasminogen activator receptor is associated with the development of adipose tissue

2010 ◽  
Vol 104 (12) ◽  
pp. 1124-1132 ◽  
Author(s):  
Hiroyuki Matsuno ◽  
Eri Kawashita ◽  
Kiyotaka Okada ◽  
Hidetaka Suga ◽  
Shigeru Ueshima ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator ◽  
Adipocyte Differentiation ◽  
Cellular Adhesion ◽  
Wild Type ◽  
Tissue Mass ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Plasminogen Activator Receptor

SummaryUrokinase-type plasminogen activator receptor (uPAR) plays a role in cellular responses which include cellular adhesion, differentiation, proliferation and migration. The aim of this study was to clarify the role of uPAR on the development of adipose tissue. To clarify the role of uPAR on adipogenesis, we examined the effect of uPAR overexpression and uPAR deficiency on the adipocyte differentiation. Adipocyte differentiation was induced by incubation of 3T3-L1 cells with differentiation media containing insulin, dexamethasone, and 1-methyl-3-isobutylxanthin. uPAR overexpression by transfection of uPAR expression vector induced adipocyte differentiation. In addition, we examined the difference in adipocyte differentiation of mesenchymal stem cells from wild-type mice and uPAR knockout (uPAR-/-) mice. The uPAR deficiency attenuated differentiation media-induced adipocyte differentiation. Moreover, we found that the inhibition of phosphatidylinositol 3-kinase (PI3K) pathway attenuated uPAR overexpression-induced adipocyte differentiation, and uPAR overexpression induced the activation of Akt. We also found that an increase of the adipose tissue mass in uPAR-/- mice was less than that observed in wild-type mice. The present results suggest that uPAR plays a pivotal role in the development of adipose tissue through PI3K/Akt pathway.

scholarly journals JAZF1 heterozygous knockout mice show altered adipose development and metabolism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jain Jeong ◽  
Soyoung Jang ◽  
Song Park ◽  
Wookbong Kwon ◽  
Si-Yong Kim ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Knockout Mice ◽  
Metabolic Disorders ◽  
Adipocyte Differentiation ◽  
Zinc Finger Protein ◽  
Tissue Mass ◽  
In Vivo Models ◽  
Brown Adipose

Abstract Background Juxtaposed with another zinc finger protein 1 (JAZF1) is associated with metabolic disorders, including type 2 diabetes mellitus (T2DM). Several studies showed that JAZF1 and body fat mass are closely related. We attempted to elucidate the JAZF1 functions on adipose development and related metabolism using in vitro and in vivo models. Results The JAZF1 expression was precisely regulated during adipocyte differentiation of 3T3-L1 preadipocyte and mouse embryonic fibroblasts (MEFs). Homozygous JAZF1 deletion (JAZF1-KO) resulted in impaired adipocyte differentiation in MEF. The JAZF1 role in adipocyte differentiation was demonstrated by the regulation of PPARγ—a key regulator of adipocyte differentiation. Heterozygous JAZF1 deletion (JAZF1-Het) mice fed a normal diet (ND) or a high-fat diet (HFD) had less adipose tissue mass and impaired glucose homeostasis than the control (JAZF1-Cont) mice. However, other metabolic organs, such as brown adipose tissue and liver, were negligible effect on JAZF1 deficiency. Conclusion Our findings emphasized the JAZF1 role in adipocyte differentiation and related metabolism through the heterozygous knockout mice. This study provides new insights into the JAZF1 function in adipose development and metabolism, informing strategies for treating obesity and related metabolic disorders.

Abstract 1376: The Nadph Oxidase Nox4 Controls Mkp1 Expression and Thereby the Development of White Adipose Tissue

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Katrin Schröder ◽  
Judith G Schreiber ◽  
Ralf P Brandes
Keyword(s):  
Adipose Tissue ◽  
Risk Factor ◽  
Cardiovascular Risk ◽  
Nadph Oxidase ◽  
Opposite Effect ◽  
Adipocyte Differentiation ◽  
Underlying Mechanism ◽  
3T3 Fibroblasts ◽  
Proliferation And Differentiation

Obesity is a cardiovascular risk factor. Insulin promotes the formation of adipocytes by promoting fibroblast into adipocyte differentiation. Insulin however also acts as a mitogen for fibroblasts and the balance of insulin-induced proliferation and differentiation is incompletely understood. We hypothesize that the NADPH oxidase Nox4 acts as a central switch between these two processes. In 3T3-fibroblasts Nox4 siRNA reduced the cellular radical formation and attenuated the insulin-stimulated differentiation from fibroblasts into adipocytes. Importantly, insulin-induced proliferation was enhanced by Nox4 siRNA. Accordingly, Nox4 overexpression enhanced differentiation and reduced insulin-stimulated proliferation. We generated Nox4 knockout mice to study the in vivo relevance of this observation: The amount of adipose tissue was reduced in the Nox4−/− animals as compared to their wildtype littermates suggesting indeed an attenuated adipocyte differentiation, whereas fibroblasts obtained from Nox4−/− mice presented with enhanced proliferation. To uncover the underlying mechanism, we focused on the Erk1/2 pathway. Erk1/2 signaling is prevented by dephosphorylation through the dualspecific phosphatase MKP1. Luciferase reportergene assays using the full-length MKP1 promotor revealed that Nox4 siRNA reduced, and overexpression of Nox4 as well as treatment of the cells with H 2 O 2 induced MKP1 promotor activity. Indeed, Nox4 siRNA reduced MKP1 protein expression and thus enhanced basal and insulin-induced activation of Erk1/2 in fibroblasts. Nox4 overexpression had the opposite effect. Importantly, MKP1 expression was also reduced in adipose tissue from Nox4−/− mice. Overexpression of MKP1 in fibroblastes increased insulin-induced differentiation and attenuated proliferation, whereas MKP1 siRNA had the opposite effect. We conclude that Nox4, by regulating MKP1, is essentially involved in adipocyte differentiation and development of obesity.

Abstract 339: Impaired Periaortic Adipocyte Differentiation in Angiotensin AT1 Receptor-Deficient Mice: Possible Role in Proinflammatory Phenotypic Modulation of Perivascular Adipose Tissue

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Daisuke Irie ◽  
Hiroyuki Yamada ◽  
Taku Kato ◽  
Hiroyuki Kawahito ◽  
Kouji Ikeda ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
At1 Receptor ◽  
Brown Adipocyte ◽  
Marker Genes ◽  
Interscapular Brown Adipose Tissue ◽  
Perivascular Adipose Tissue ◽  
Expression Levels ◽  
Brown Adipose ◽  
Differentiation Marker

[BACKGROUND] The angiotensin II type 1 (AT1) receptor in visceral white adipose tissue (WAT) is closely implicated in lipid metabolism and energy homeostasis. Recently, perivascular adipose tissue (PVAT) has been shown to play a crucial role in the development of atherosclerosis; however, the effects of AT1 on PVAT properties and their functional relevance in atherogenesis remain undefined. [METHOD AND RESULT] We examined the fat depot-specific difference of adipose tissue among epididymal WAT, PVAT surrounding thoracic aorta, and interscapular brown adipose tissue (BAT) in 8-week-old apoE deficient (apoE-/-) mice. The expression levels of brown adipocyte marker genes (UCP-1, PGC-1α, Elovl3, PPARα, and Cidea) were significantly higher in BAT and PVAT compared with WAT (P<0.01). White adipocyte marker genes (Igfbp3, DPT, Tcf21, and Hoxc9), which were hardly expressed in BAT, showed a moderate expression levels in PVAT, suggesting that PVAT has a strikingly different phenotype from the classical WAT and BAT. We next examined the properties of PVAT in 8-week-old apoE-/-/AT1 receptor deficient (Agtr1-/-) mice. After 4 weeks of western diet, the expression levels of adipocyte differentiation maker genes (PPARγ, FABP4, c/EBPα) were markedly increased in apoE -/- PVAT (P<0.05), which was completely diminished in apoE-/-/Agtr1 -/- PVAT (P<0.01). To investigate the effect of AT1 on the periaortic adipocyte differentiation, we performed primary culture of preadipocyte from stromal vascular fraction in Agtr1 -/- and Agtr1+/+ PVAT. The mRNA expressions of adipocyte differentiation marker genes (PPARγ, FABP4, and c/EBPα) were time-dependently increased in Agtr1+/+ adipocyte. In contrast, FABP4 and c/EBPα mRNA expressions were markedly inhibited in Agtr1 -/- adipocyte, whereas PPARγ did not differ between the two groups during differentiation, suggesting that AT1 is essentially implicated in the terminal differentiation of periaortic adipocyte. [CONCLUSION] Our findings demonstrate that AT1 regulates the expression levels of late stage of adipocyte-differentiation marker genes in PVAT, suggesting that AT1-mediated modulation of periaortic adipocyte differentiation could be a novel therapeutic target for the prevention of atherosclerosis.

scholarly journals Generation of immune cell containing adipose organoids for in vitro analysis of immune metabolism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jacqueline Taylor ◽  
Julia Sellin ◽  
Lars Kuerschner ◽  
Lennart Krähl ◽  
Yasmin Majlesain ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Immune Cell ◽  
Stromal Vascular Fraction ◽  
Cell Populations ◽  
Endocrine Organ ◽  
Vitro Analysis ◽  
In Vitro Analysis ◽  
Better Than

AbstractAdipose tissue is an organized endocrine organ with important metabolic and immunological functions and immune cell-adipocyte crosstalk is known to drive various disease pathologies. Suitable 3D adipose tissue organoid models often lack resident immune cell populations and therefore require the addition of immune cells isolated from other organs. We have created the first 3D adipose tissue organoid model which could contain and maintain resident immune cell populations of the stromal vascular fraction (SVF) and proved to be effective in studying adipose tissue biology in a convenient manner. Macrophage and mast cell populations were successfully confirmed within our organoid model and were maintained in culture without the addition of growth factors. We demonstrated the suitability of our model for monitoring the lipidome during adipocyte differentiation in vitro and confirmed that this model reflects the physiological lipidome better than standard 2D cultures. In addition, we applied mass spectrometry-based lipidomics to track lipidomic changes in the lipidome upon dietary and immunomodulatory interventions. We conclude that this model represents a valuable tool for immune-metabolic research.

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