2.P.7 Age-related decline in plasma CETP and CETP mRNA expression in human adipose tissue

1997 ◽  
Vol 134 (1-2) ◽  
pp. 118
Author(s):  
T. Radeau ◽  
M. Robb ◽  
P. Lau ◽  
J. Borthwick ◽  
R. McPherson
1999 ◽  
Vol 54 (5) ◽  
pp. B183-B188 ◽  
Author(s):  
K. Hotta ◽  
N. L. Bodkin ◽  
T. A. Gustafson ◽  
S. Yoshioka ◽  
H. K. Ortmeyer ◽  
...  

2000 ◽  
pp. 195-199 ◽  
Author(s):  
R Peino ◽  
V Pineiro ◽  
O Gualillo ◽  
C Menendez ◽  
J Brenlla ◽  
...  

OBJECTIVE: Leptin secretion is reduced by low temperatures in experimental animals, and this effect has been explained as an adaptive mechanism to cold environments. This study investigated the in vitro effects of cold exposure on human white adipose tissue. DESIGN: To understand whether the low temperature action is a direct or a mediated effect, leptin secretion was assessed in vitro in human omental adipose tissue incubated at varied temperatures, from 38 donors. As an internal control, the effect of reduced temperatures on in vitro GH secretion by GH3 cells was assessed. METHODS: Measurement of hormones secretion was carried out with an RIA, while human ob gene mRNA expression was assessed with reverse transcription PCR. RESULTS: Compared with the standard temperature of 37 degrees C, leptin secretion by human adipose tissue was significantly (P<0.05) reduced when the incubations were carried out at 34.5 degrees C (41% inhibition), and 32 degrees C (68% inhibition), with no parallel changes in the ob mRNA expression. At these reduced temperatures, glucocorticoid-mediated leptin secretion was well preserved. When the effect of reduced temperatures was assessed on in vitro GH secretion, a superimposable reduction was observed. CONCLUSIONS: These results indicate: (i) that low temperatures reduce leptin secretion by acting directly on the adipose tissue and (ii) that the similar reduction in a hormone unrelated to energy metabolism, such as GH, suggests that the observed reduction is a mechanical perturbation of leptin secretion, which may be devoid of physiological implications.


2020 ◽  
Author(s):  
Weiguo Lao ◽  
Yi Tan ◽  
Michael Johnson ◽  
Yan Li ◽  
Yiguang Lin ◽  
...  

Abstract Background: Osteoporosis is a metabolic disease affecting the bone mineral density associated with increased adiposity in the aging population with obesity. The nutrients to control osteoblast and adipocyte differentiation from a common precursor, the pluripotent mesenchymal stem cell (MSC), may be a promising therapy for osteoporosis. Previously, we have shown that green tea polyphenols (GTP) exert anti-adipogenic effects on preadipocyte proliferation. In the present study, we investigated regulatory effects of GTP on osteogenesis and adipogenesis during early differentiation of human adipose tissue-derived stem cells (hADSCs). Methods: GTP at concentrations of 1 and 10 µg/ml was incubated with primary hADSCs in presence or absence of pioglitazone (100 µmol) during hADSCs differentiation. Adipogenesis of hADSCs was determined by Oil Red O staining and measurement of the cellular triglyceride synthesis in mature adipocyte. Alkaline phosphatase (ALP) assay and the measurement of intracellular calcium were utilized to determine osteoporosis of hADSCs. Immunofluorescence staining and qRT-PCR were employed to detect PPARγ-CEBPA regulated adipogenic pathway and the RUNX2-BMP2 mediated osteogenic pathway. Results: GTP treatment significantly decreased lipid accumulation and the cellular triglyceride synthesis in mature adipocytes and attenuated pioglitazone-induced adipogenesis in a dose-dependent manner. GTP downregulated protein and mRNA expression of Pparγ and attenuated pioglitazone-stimulated Cebpa expression in mature adipocytes. Concurrently, measurements of calcium content and ALP activity showed that GTP treatment significantly enhanced hADSCs differentiation into osteocytes compared with the control and pioglitazone-treated cells. Meanwhile, GTP upregulated protein and mRNA expression of RunX2 and Bmp2 compared to the control and GTP at 10 µg/mL significantly attenuated the decreased mRNA expression of Runx2 and Bmp2 by pioglitazone. Conclusions: The present study demonstrated that GTP possess a greater ability to facilitate osteogenesis and simultaneously inhibit hADSCs differentiation into the adipogenic lineage through upregulating the RUNX2-BMP2 mediated osteogenic pathway and suppressing PPARγ-induced signaling of adipogenesis. The findings of this study highlight that GTP may be a therapeutic intervention to combat osteoporosis associated obesity.


2021 ◽  
Author(s):  
Valéria Ferreira-Silva ◽  
Munira M. A. Baqui ◽  
Greice A. Molfetta ◽  
Aparecida M. Fontes ◽  
Dalila I. Zanette ◽  
...  

AbstractDNA methylation patterns are closely related to the chromatin structure, and its remodeling is considered an important mechanism in the control of gene transcription during cell differentiation. In rodent, several studies have related the possibility that multipotent mesenchymal stromal cells (MSCs) undergo cardiomyogenesis. However, it has not been completely elucidated if human adult stem cell exhibits true differentiation potential for a cardiac lineage. In this study, the action of the DNA methylation inhibitor 5-azacytidine (5-aza) was examined in human adipose tissue pericytes (hATPCs: 3G5+) regarding their possible capacity to induce myocytes in vitro. Real-Time PCR revealed that cells treated with 5-aza presented time-dependent decrease in the mRNA expression of α-cardiac actin (α-CA). At 24 h, this diminution was statistically significant; however, there was not a correlation with the highest level of DNA demethylation at the same period using Methylation-Sensitive High Resolution Melting-PCR (MS-HRM-PCR). An evident increase in the α-CA protein expression was observed by Western blotting in hATPCs treated with 5-aza at 24 h. The mRNA expression of α-SMA (α-smooth actin) also showed a time-dependent decrease after the treatment, however, it was not significant. The ultrastructural analysis showed similar structures such as like-cell junctions, caveolae, and actin myofilaments, which aligned in parallel. These phenotypic alterations were found only after the treatment; however, the hTAPCs after 5-aza treatment were not able to form thick myofilaments and consequently sarcomeres. These results indicated that a terminal cardiac differentiation of hTAPCs was not achieved and that the cardiomyogenesis failure could be related to the non-muscle origin of the adipose tissue.


2006 ◽  
Vol 191 (1) ◽  
pp. 129-136 ◽  
Author(s):  
J E Digby ◽  
J Chen ◽  
J Y Tang ◽  
H Lehnert ◽  
R N Matthews ◽  
...  

Orexin-A and orexin-B, via their receptors orexin-1 receptor (OX1R) and orexin-2 receptor (OX2R) have been shown to play a role in the regulation of feeding, body weight, and energy expenditure. Adipose tissue also contributes significantly to the maintenance of body weight by interacting with a complex array of bioactive peptides; however, there are no data as yet on the expression of orexin components in adipose tissue. We, therefore, analyzed the expression of OX1R and OX2R in human adipose tissue and determined functional responses to orexin-A and orexin-B. OX1R and OX2R mRNA expression was detected in subcutaneous (s.c.) and omental adipose tissue and in isolated adipocytes. Protein for OX1R and OX2R was also detected in whole adipose tissue sections and lysates. Treatment with orexin-A, and orexin-B (100 nM, 24 h) resulted in a significant increase in peroxisome proliferator-activated receptors γ-2 mRNA expression in s.c. adipose tissue (P < 0.05). Hormone sensitive lipase mRNA was significantly reduced in omental adipose tissue with orexin-A and orexin-B treatment (P < 0.05). Glycerol release from omental adipose tissue was also significantly reduced with orexin-A treatment (P < 0.05). These findings demonstrate for the first time the presence of functional orexin receptors in human adipose tissue and suggest a role for orexins in adipose tissue metabolism and adipogenesis.


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