scholarly journals Time course transcriptomic analysis of adipogenic differentiation of human white adipose tissue (WAT)-derived stromal cells

2017 ◽  
Author(s):  
MA Ambele ◽  
C Dessels ◽  
C Durandt ◽  
MS Pepper
2020 ◽  
Vol 21 (24) ◽  
pp. 9694
Author(s):  
Lucio Díaz-Flores ◽  
Ricardo Gutiérrez ◽  
Ma Pino García ◽  
Miriam González-Gómez ◽  
Jose Luís Carrasco ◽  
...  

We studied telocytes/CD34+ stromal cells (TCs/CD34+SCs) in pathologically affected white adipose tissue after briefly examining them in normal fat. To this aim, we reviewed pathological processes, including original contributions, in which TCs/CD34+SCs are conserved, increased, and lost, or acquire a specific arrangement. The pathologic processes in which TCs/CD34+SCs are studied in adipose tissue include inflammation and repair through granulation tissue, iatrogenic insulin-amyloid type amyloidosis, non-adipose tissue components (nerve fascicles and fibres in neuromas and hyperplastic neurogenic processes) and tumours (signet ring carcinoma with Krukenberg tumour and colon carcinoma) growing in adipose tissue, adipose tissue tumours (spindle cell lipoma, dendritic fibromyxolipoma, pleomorphic lipoma, infiltrating angiolipoma of skeletal muscle and elastofibrolipoma), lipomatous hypertrophy of the interatrial septum, nevus lipomatosus cutaneous superficialis of Hoffman–Zurhelle and irradiated adipose tissue of the perirectal and thymic regions. Two highly interesting issues emerged: (1) whether the loss of CD34 expression in TCs/CD34+SCs is by changes in marker expression or the disappearance of these cells (the findings suggest the first possibility) and (2) whether in some invasive and metastatic malignant tumours, TCs/CD34+SCs that completely surround neoplastic cells act as nurse and/or isolating cells. Further studies are required on adipose tissue TCs/CD34+SCs, mainly in lipomatosis and obesity.


2019 ◽  
Vol 20 (7) ◽  
pp. 1618 ◽  
Author(s):  
Abeer Fayyad ◽  
Amir Khan ◽  
Sallam Abdallah ◽  
Sara Alomran ◽  
Khalid Bajou ◽  
...  

Obesity is a major risk for diabetes. Brown adipose tissue (BAT) mediates production of heat while white adipose tissue (WAT) function in the storage of fat. Roles of BAT in the treatment of obesity and related disorders warrants more investigation. Peroxisome proliferator activator receptor gamma (PPAR-γ) is the master regulator of both BAT and WAT adipogenesis and has roles in glucose and fatty acid metabolism. Adipose tissue is the major expression site for PPAR-γ. In this study, the effects of rosiglitazone on the brown adipogenesis and the association of MAPK and PI3K pathways was investigated during the in vitro adipogenic differentiation of telomerase transformed mesenchymal stromal cells (iMSCs). Our data indicate that 2 µM rosiglitazone enhanced adipogenesis by over-expression of PPAR-γ and C/EBP-α. More specifically, brown adipogenesis was enhanced by the upregulation of EBF2 and UCP-1 and evidenced by multilocular fatty droplets morphology of the differentiated adipocytes. We also found that rosiglitazone significantly activated MAPK and PI3K pathways at the maturation stage of differentiation. Overall, the results indicate that rosiglitazone induced overexpression of PPAR-γ that in turn enhanced adipogenesis, particularly browning adipogenesis. This study reports the browning effects of rosiglitazone during the differentiation of iMSCs into adipocytes in association with the activation of MAPK and PI3K signaling pathways.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1603-1603
Author(s):  
Mehrnaz Abbasi ◽  
Shu Wang

Abstract Objectives Obesity and its comorbidities are major public health problems worldwide. The transformation of white adipose tissue (WAT) to brown adipose tissue (BAT); browning of WAT, may serve as a promising strategy for combating obesity. Metformin is not only the first line of drug for type 2 diabetes but also has an anti-obesity potential. Emerging evidence suggests that metformin can reduce body weight and enhance energy expenditure via activating BAT or browning of WAT. However, metformin delivery to adipose tissue is limited due to the lack of adipocyte-specific surface markers. Thus, the direct injection might be an alternative. Methods ApoE3-Leiden.human cholesteryl ester transfer protein (E3L.CETP) mice (5 mice/group) were fed a high-fat diet (HFD) for 15 weeks. From week 10 to 15, mice were randomly divided into 3 groups as 1. Metformin inguinal WAT (IgWAT) injection, 2. Metformin delivery to interscapular BAT (IBAT) and 3. Saline IgWAT injection (HFD control). Mice received injections twice per week (40 mg/kg/week). Bodyweight (BW), body composition, food intake, energy expenditure and glucose tolerance test (GTT) were measured. Gene expression of beige or brown makers was analyzed using real time-PCR. Results Compared to HFD control mice, IgWAT- and IBAT-treated mice lost 2.16% and 1.9% more of their body fat, respectively (P-value < 0.001). IgWAT- and IBAT-treated mice had 1.09- and 1.24-fold lower area under the curve calculated from the GTT time course than HFD control mice, respectively, but the differences were not statistically significant. The metabolic cage data indicated that both IgWAT- and IBAT-treated mice compared to HFD control mice had significantly decreased respiration exchange ratio (RER) (P < 0.0001). IgWAT-treated mice had significantly lower IgWAT weight than the HFD control mice (P < 0.05). IgWAT-treated compared to HFD control mice had 1.5-, 2-, 2.7- and 3-fold higher expression of UCP1, PRDM16, TMEM26 and Elovl3 in IgWAT, respectively. Conclusions This study demonstrated that local delivery of metformin to IgWAT and IBAT decreased BW and fat mass, which were associated with reduced RER and improved glucose homeostasis. Direct delivery of metformin to IgWAT and IBAT might be an efficient approach for combating obesity via inducing IgWAT browning and enhancing IBAT activity. Funding Sources NIH 1R15AT010395 and AHA 19AIREA34480011.


2014 ◽  
Vol 67 (10) ◽  
pp. 1427-1435 ◽  
Author(s):  
M. Gierloff ◽  
L. Petersen ◽  
H.-H. Oberg ◽  
E.S. Quabius ◽  
J. Wiltfang ◽  
...  

2005 ◽  
Vol 289 (4) ◽  
pp. E608-E616 ◽  
Author(s):  
James G. Granneman ◽  
Pipeng Li ◽  
Zhengxian Zhu ◽  
Yuyan Lu

Selective agonists of β3-adrenergic receptors (Adrb3) exhibit potent anti-diabetes properties in rodent models when given chronically, yet the mechanisms involved are poorly understood. A salient feature of chronic Adrb3 activation is pronounced remodeling of white adipose tissue (WAT), which includes mitochondrial biogenesis and elevation of metabolic rate. To gain insights into potential mechanisms underlying WAT remodeling, the time course of remodeling induced by the Adrb3 agonist CL-316,243 (CL) was analyzed using histological, physiological, and global gene profiling approaches. The results indicate that continuous CL treatment induced a transient proinflammatory response that was followed by cellular proliferation among stromal cells and multilocular adipoctyes. CL treatment strongly fragmented the central lipid storage droplet of mature adipocytes and induced mitochondrial biogenesis within these cells. Mitochondrial biogenesis was correlated with the upregulation of genes involved in fatty acid oxidation and mitochondrial electron transport activity. The elevated catabolic activity of WAT was temporally correlated with upregulation of peroxisome proliferator-activated receptor-α and its target genes, suggesting involvement of this transcription factor in coordinating the gene program that elevates WAT catabolic activity.


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