scholarly journals Peroxisome proliferator activated receptor ligands affect porcine endometrial steroids production during the estrous cycle and early pregnancy: an in vitro study

2016 ◽  
Vol 61 (08) ◽  
pp. 360-368 ◽  
Author(s):  
A. Kurzyńska ◽  
M. Bogacki ◽  
K. Chojnowska ◽  
I. Bogacka
2013 ◽  
Vol 13 ◽  
pp. 42-43
Author(s):  
Patrycja Młotkowska ◽  
Agnieszka Skowrońska ◽  
Leszek Frąckowiak ◽  
Mariusz T. Skowroński

2019 ◽  
Vol 20 (8) ◽  
pp. 1862 ◽  
Author(s):  
Orlando ◽  
Chimienti ◽  
Pesce ◽  
Fracasso ◽  
Lezza ◽  
...  

Dietary gliadin may show a broad spectrum of toxicity. The interplay between mitochondria and gliadin-induced oxidative stress has not been thoroughly examined in the intestinal epithelium. In this kinetic study, Caco-2 cells were exposed for 24 h to pepsin-trypsin-digested gliadin, alone or in combination with the antioxidant 2,6-di-tbutyl-p-cresol (BHT), and the effects on mitochondrial biogenesis and mtDNA were studied. Cells ability to recover from stress was determined after 24 h and 48 h of incubation in the culture medium. Gliadin-induced oxidative stress evoked a compensatory response. The stressor triggered a rapid and significant increase of Peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and Peroxiredoxin III (PrxIII) proteins, and mtDNA amount. As for the effects of gliadin on mtDNA integrity, strand breaks, abasic sites, and modified bases were analyzed in three mtDNA regions. D-loop appeared a more fragile target than Ori-L and ND1/ND2. The temporal trend of the damage at D-loop paralleled that of the amount of mtDNA. Overall, a trend toward control values was shown 48 h after gliadin exposure. Finally, BHT was able to counteract the effects of gliadin. Results from this study highlighted the effects of gliadin-induced oxidative stress on mitochondria, providing valuable evidence that might improve the knowledge of the pathophysiology of gluten-related disorders.


2019 ◽  
Vol 161 (5) ◽  
pp. 1017-1024
Author(s):  
Stefan Linsler ◽  
Ralf Ketter ◽  
Joachim Oertel ◽  
Steffi Urbschat

2016 ◽  
Vol 242 (10) ◽  
pp. 1079-1085 ◽  
Author(s):  
Ignazio Barbagallo ◽  
Giovanni Li Volti ◽  
Fabio Galvano ◽  
Guido Tettamanti ◽  
Francesca R Pluchinotta ◽  
...  

Adipose tissue dysfunction represents a hallmark of diabetic patients and is a consequence of the altered homeostasis of this tissue. Mesenchymal stem cells (MSCs) and their differentiation into adipocytes contribute significantly in maintaining the mass and function of adult adipose tissue. The aim of this study was to evaluate the differentiation of MSCs from patients suffering type 2 diabetes (dASC) and how such process results in hyperplasia or rather a stop of adipocyte turnover resulting in hypertrophy of mature adipocytes. Our results showed that gene profile of all adipogenic markers is not expressed in diabetic cells after differentiation indicating that diabetic cells fail to differentiate into adipocytes. Interestingly, delta like 1, peroxisome proliferator-activated receptor alpha, and interleukin 1β were upregulated whereas Sirtuin 1 and insulin receptor substrate 1 gene expression were found downregulated in dASC compared to cells obtained from healthy subjects. Taken together our data indicate that dASC lose their ability to differentiate into mature and functional adipocytes. In conclusion, our in vitro study is the first to suggest that diabetic patients might develop obesity through a hypertrophy of existing mature adipocytes due to failure turnover of adipose tissue. Impact statement In the present manuscript, we evaluated the differentiative potential of mesenchymal stem cells (MSCs) in adipocytes obtained from healthy and diabetic patients. This finding could be of great potential interest for the field of obesity in order to exploit such results to further understand the pathophysiological processes underlying metabolic syndrome. In particular, inflammation in diabetic patients causes a dysfunction in MSCs differentiation and a decrease in adipocytes turnover leading to insulin resistance.


Author(s):  
Daniela Soto ◽  
Claudia Martini ◽  
Evelyn Frontera ◽  
Laura Montaldo ◽  
Maria C. Vila ◽  
...  

Aims: Reports regarding the effects of antioxidants in obesity have been contradictory. Antioxidant N-acetylcysteine is usually considered a nutritional supplement. Our aim is to evaluate bioactivity of N-acetylcysteine (NAC) on mature adipocytes, which is a close model to in vivo condition. Study Design: In vitro study. Place and Duration of Study: Department of Basic Science (Universidad Nacional de Lujan), Department of Chemical Biology (Universidad de Buenos Aires), CONICET – INEDES and CONICET – IQUIBICEN, between March 2017 and June 2019. Methodology: We evaluated the bioactivity of different concentrations of NAC for 5 days (0.01 mM to 5 mM) on fully differentiated 3T3-L1 cells (mature adipocytes). Results: We demonstrated that NAC treatment was not toxic to mature adipocytes. Only 5mM NAC inhibited reactive oxygen species production. 5 mM NAC treatment resulted in a 60% decrease in cellular triglycerides content and inhibited 70% cholesterol accumulation.  We also determined the mRNA and protein expression levels of Peroxisome Proliferator-Activated Receptor g as well as, mRNA levels of lipid protein Perilipin in NAC treated adipocytes; we observed that 5mM NAC treatment caused nearly 30% decrease in the expression of these parameters. Conclusion: These results suggest that NAC could avoid lipid accumulation in mature adipocytes; the antioxidant NAC could be beneficial in obesity treatment.


2013 ◽  
Vol 43 (2) ◽  
pp. 409-420 ◽  
Author(s):  
S. Lea ◽  
J. Plumb ◽  
H. Metcalfe ◽  
D. Spicer ◽  
P. Woodman ◽  
...  

2011 ◽  
Vol 8 (1) ◽  
pp. 114 ◽  
Author(s):  
Liu Tao ◽  
Chen Suhua ◽  
Chen Juanjuan ◽  
Yin Zongzhi ◽  
Xiao Juan ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document