scholarly journals Depletion of white adipocyte progenitors induces beige adipocyte differentiation and suppresses obesity development

2014 ◽  
Vol 22 (2) ◽  
pp. 351-363 ◽  
Author(s):  
A C Daquinag ◽  
C Tseng ◽  
A Salameh ◽  
Y Zhang ◽  
F Amaya-Manzanares ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Beige Adipocyte ◽  
White Adipocyte ◽  
Adipocyte Progenitors

scholarly journals Aquaglyceroporins Are Differentially Expressed in Beige and White Adipocytes

2020 ◽  
Vol 21 (2) ◽  
pp. 610
Author(s):  
Inês Vieira da Silva ◽  
Francisco Díaz-Sáez ◽  
António Zorzano ◽  
Anna Gumà ◽  
Marta Camps ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Expression Patterns ◽  
Physiological Role ◽  
Glycerol Metabolism ◽  
Metabolic Complications ◽  
Altered Expression ◽  
Beige Adipocyte ◽  
White Adipocyte ◽  
White Adipocytes

Browning of white adipocytes has been proposed as a powerful strategy to overcome metabolic complications, since brown adipocytes are more catabolic, expending energy as a heat form. However, the biological pathways involved in the browning process are still unclear. Aquaglyceroporins are a sub-class of aquaporin water channels that also permeate glycerol and are involved in body energy homeostasis. In the adipose tissue, aquaporin-7 (AQP7) is the most representative isoform, being crucial for white adipocyte fully differentiation and glycerol metabolism. The altered expression of AQP7 is involved in the onset of obesity and metabolic disorders. Herein, we investigated if aquaglyceroporins are implicated in beige adipocyte differentiation, similar to white cells. Thus, we optimized a protocol of murine 3T3-L1 preadipocytes browning that displayed increased beige and decreased white adipose tissue features at both gene and protein levels and evaluated aquaporin expression patterns along the differentiation process together with cellular lipid content. Our results revealed that AQP7 and aquaporin-9 (AQP9) expression was downregulated throughout beige adipocyte differentiation compared to white differentiation, which may be related to the beige physiological role of heat production from oxidative metabolism, contrasting with the anabolic/catabolic lipid metabolism requiring glycerol gateways occurring in white adipose cells.

RANKL induces beige adipocyte differentiation in preadipocytes

2020 ◽  
Vol 318 (6) ◽  
pp. E866-E877
Author(s):  
Flávia Sayuri Matsuo ◽  
Paulo Henrique Cavalcanti de Araújo ◽  
Ryerson Fonseca Mota ◽  
Ana Júlia Rossoni Carvalho ◽  
Mariana Santos de Queiroz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Stromal Vascular Fraction ◽  
Nuclear Factor Κb ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Marker Genes ◽  
Beige Adipocyte ◽  
White Adipocyte

The receptor activator of nuclear factor-κB (NF-κB) (RANK), its ligand (RANKL), and the decoy receptor osteoprotegerin (OPG) are a triad of proteins that regulate bone metabolism, and serum OPG is considered a biomarker for cardiovascular diseases and Type 2 diabetes; however, the implications of OPG in adipose tissue metabolism remains elusive. In this study, we investigate RANK-RANKL-OPG signaling in white adipose tissue browning. Histological analysis of osteoprotegerin knockout (OPG−/−) mice showed subcutaneous white adipose tissue (sWAT) browning, resistance for high-fat diet-induced weight gain, and preserved glucose metabolism compared with wild-type (WT) mice. Stromal vascular fraction (SVF) cells from sWAT of OPG−/− mice showed multilocular morphology and higher expression of brown adipocyte marker genes compared with those from the WT group. Infusion of RANKL induced browning and elevated respiratory rates in sWAT, along with increased whole body oxygen consumption in mice measured by indirect calorimetry. Subcutaneous WAT-derived SVF and 3T3-L1 cells, but not mature white adipocytes, differentiated into beige adipose tissue in the presence of RANKL. Moreover, SVF cells, even under white adipocyte differentiation, showed multilocular lipid droplet, lower lipid content, and increased expression of beige adipocyte markers with RANKL stimulation. In this study, we show for the first time the contribution of RANKL to increase energy expenditure by inducing beige adipocyte differentiation in preadipocytes.

Aging impairs beige adipocyte differentiation of mesenchymal stem cells via the reduced expression of Sirtuin 1

2018 ◽  
Vol 500 (3) ◽  
pp. 682-690 ◽  
Author(s):  
Vuong Cat Khanh ◽  
Amin Firman Zulkifli ◽  
Chiho Tokunaga ◽  
Toshiharu Yamashita ◽  
Yuji Hiramatsu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipocyte Differentiation ◽  
Sirtuin 1 ◽  
Beige Adipocyte

scholarly journals CD90 Is Dispensable for White and Beige/Brown Adipocyte Differentiation

2020 ◽  
Vol 21 (21) ◽  
pp. 7907
Author(s):  
Meike Dahlhaus ◽  
Julian Roos ◽  
Daniel Engel ◽  
Daniel Tews ◽  
Daniel Halbgebauer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Stromal Cells ◽  
Adipocyte Differentiation ◽  
Human Adipose Tissue ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Brown Adipose ◽  
Adipose Tissue Stromal Cells ◽  
Flow Cytometric Sorting

Brown adipose tissue (BAT) is a thermogenic organ in rodents and humans. In mice, the transplantation of BAT has been successfully used to combat obesity and its comorbidities. While such beneficial properties of BAT are now evident, the developmental and cellular origins of brown, beige, and white adipocytes have remained only poorly understood, especially in humans. We recently discovered that CD90 is highly expressed in stromal cells isolated from human white adipose tissue (WAT) compared to BAT. Here, we studied whether CD90 interferes with brown or white adipogenesis or white adipocyte beiging. We applied flow cytometric sorting of human adipose tissue stromal cells (ASCs), a CRISPR/Cas9 knockout strategy in the human Simpson-Golabi-Behmel syndrome (SGBS) adipocyte model system, as well as a siRNA approach in human approaches supports the hypothesis that CD90 affects brown or white adipogenesis or white adipocyte beiging in humans. Taken together, our findings call the conclusions drawn from previous studies, which claimed a central role of CD90 in adipocyte differentiation, into question.

scholarly journals The Forkhead Transcription Factor FoxC2 Inhibits White Adipocyte Differentiation

2004 ◽  
Vol 279 (41) ◽  
pp. 42453-42461 ◽  
Author(s):  
Kathryn E. Davis ◽  
Marthe Moldes ◽  
Stephen R. Farmer
Keyword(s):  
Transcription Factor ◽  
Adipocyte Differentiation ◽  
Forkhead Transcription Factor ◽  
White Adipocyte

scholarly journals Increased prostaglandin-D2 in male STAT3-deficient hearts shifts cardiac progenitor cells from endothelial to white adipocyte differentiation

PLoS Biology ◽  
2020 ◽  
Vol 18 (12) ◽  
pp. e3000739
Author(s):  
Elisabeth Stelling ◽  
Melanie Ricke-Hoch ◽  
Sergej Erschow ◽  
Steve Hoffmann ◽  
Anke Katharina Bergmann ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Adipocyte Differentiation ◽  
Young Male ◽  
Conditional Knockout ◽  
Prostaglandin D2 ◽  
Cardiac Progenitor Cells ◽  
White Adipocyte ◽  
Female Mice ◽  
Age Related ◽  
Ezh2 Expression

Cardiac levels of the signal transducer and activator of transcription factor-3 (STAT3) decline with age, and male but not female mice with a cardiomyocyte-specific STAT3 deficiency conditional knockout (CKO) display premature age-related heart failure associated with reduced cardiac capillary density. In the present study, isolated male and female CKO-cardiomyocytes exhibit increased prostaglandin (PG)-generating cyclooxygenase-2 (COX-2) expression. The PG-degrading hydroxyprostaglandin-dehydrogenase-15 (HPGD) expression is only reduced in male cardiomyocytes, which is associated with increased prostaglandin D2 (PGD2) secretion from isolated male but not female CKO-cardiomyocytes. Reduced HPGD expression in male cardiomyocytes derive from impaired androgen receptor (AR)–signaling due to loss of its cofactor STAT3. Elevated PGD2 secretion in males is associated with increased white adipocyte accumulation in aged male but not female hearts. Adipocyte differentiation is enhanced in isolated stem cell antigen-1 (SCA-1)+ cardiac progenitor cells (CPC) from young male CKO-mice compared with the adipocyte differentiation of male wild-type (WT)-CPC and CPC isolated from female mice. Epigenetic analysis in freshly isolated male CKO-CPC display hypermethylation in pro-angiogenic genes (Fgfr2, Epas1) and hypomethylation in the white adipocyte differentiation gene Zfp423 associated with up-regulated ZFP423 expression and a shift from endothelial to white adipocyte differentiation compared with WT-CPC. The expression of the histone-methyltransferase EZH2 is reduced in male CKO-CPC compared with male WT-CPC, whereas no differences in the EZH2 expression in female CPC were observed. Clonally expanded CPC can differentiate into endothelial cells or into adipocytes depending on the differentiation conditions. ZFP423 overexpression is sufficient to induce white adipocyte differentiation of clonal CPC. In isolated WT-CPC, PGD2 stimulation reduces the expression of EZH2, thereby up-regulating ZFP423 expression and promoting white adipocyte differentiation. The treatment of young male CKO mice with the COX inhibitor Ibuprofen or the PGD2 receptor (DP)2 receptor antagonist BAY-u 3405 in vivo increased EZH2 expression and reduced ZFP423 expression and adipocyte differentiation in CKO-CPC. Thus, cardiomyocyte STAT3 deficiency leads to age-related and sex-specific cardiac remodeling and failure in part due to sex-specific alterations in PGD2 secretion and subsequent epigenetic impairment of the differentiation potential of CPC. Causally involved is the impaired AR signaling in absence of STAT3, which reduces the expression of the PG-degrading enzyme HPGD.

scholarly journals Plac8 is required for White Adipocyte Differentiation in vitro and Cell Number Control in vivo

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e48767 ◽  
Author(s):  
Maria Jimenez-Preitner ◽  
Xavier Berney ◽  
Bernard Thorens
Keyword(s):  
Adipocyte Differentiation ◽  
Cell Number ◽  
White Adipocyte

scholarly journals Oxyresveratrol Increases Energy Expenditure through Foxo3a-Mediated Ucp1 Induction in High-Fat-Diet-Induced Obese Mice

2018 ◽  
Vol 20 (1) ◽  
pp. 26 ◽  
Author(s):  
Jin Choi ◽  
No-Joon Song ◽  
A Lee ◽  
Dong Lee ◽  
Min-Ju Seo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Biological Activities ◽  
Obese Mice ◽  
High Fat ◽  
White Adipocyte

The phytochemical oxyresveratrol has been shown to exert diverse biological activities including prevention of obesity. However, the exact reason underlying the anti-obese effects of oxyresveratrol is not fully understood. Here, we investigated the effects and mechanism of oxyresveratrol in adipocytes and high-fat diet (HFD)-fed obese mice. Oxyresveratrol suppressed lipid accumulation and expression of adipocyte markers during the adipocyte differentiation of 3T3-L1 and C3H10T1/2 cells. Administration of oxyresveratrol in HFD-fed obese mice prevented body-weight gains, lowered adipose tissue weights, improved lipid profiles, and increased glucose tolerance. The anti-obese effects were linked to increases in energy expenditure and higher rectal temperatures without affecting food intake, fecal lipid content, and physical activity. The increased energy expenditure by oxyresveratrol was concordant with the induction of thermogenic genes including Ucp1, and the reduction of white adipocyte selective genes in adipose tissue. Furthermore, Foxo3a was identified as an oxyresveratrol-induced gene and it mimicked the effects of oxyresveratrol for induction of thermogenic genes and suppression of white adipocyte selective genes, suggesting the role of Foxo3a in oxyresveratrol-mediated anti-obese effects. Taken together, these data show that oxyresveratrol increases energy expenditure through the induction of thermogenic genes in adipose tissue and further implicates oxyresveratrol as an ingredient and Foxo3a as a molecular target for the development of functional foods in obesity and metabolic diseases.

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