Circulating factors present in the sera of naturally skinny people may influence cell commitment and adipocyte differentiation of mesenchymal stromal cells

BACKGROUND Research on physiopathology of obesity may receive new hints from studies on skinny people(SP). These are individuals who show a poor or null gaining of body weight, in spite of high-calorie intake, by far exceeding the body requirements.AIM To evaluate how circulating factors present in the SP sera may affect adipogenesis of mesenchymal stromal cells(MSCs).METHODS We isolated MSCs from bone marrow of healthy donors with both normal body mass index(BMI) and caloric consumption. MSC cultures were primed with sera collected from SP or normal people(NP). Then biomolecular assays were performed to evaluate effect on proliferation, apoptosis, senescence, cell commitment, and differentiation.RESULTS SP priming affected adipocyte cell commitment and reduced spontaneous adipogenesis. Moreover, an in-depth analysis of exogenous-induced adipocyte differentiation showed striking differences between differentiation in SP-primed samples compared with NP ones. In adipocytes from SP cultures we observed a reduced size of lipid droplets, an increased expression of adipose triglyceride lipase, along with high mitochondria content and ability to produce ATP in starvation condition. These data and the expression of UCP1 protein, indicated that SP pretreatment produced a bias toward brown adipocyte differentiation.CONCLUSION Our data suggest that sera from SP may promote brown adipogenesis rather that white adipocyte differentiation. This finding could explain why SP present normal body composition in spite of an excess of caloric intake. We hypothesize that some circulating components present in the blood of these individuals may favor brown adipogenesis at expense of white adipocyte production.

Placental Vascularization and Apoptosis in Rats Orally Exposed to Low Doses of Bisphenol A

Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placental tissue through the evaluation of its effects on micro-vessel density and apoptosis. Methods: After fertilization, we exposed 3 female rats to oral BPA, by means of a free access to a beverage solution containing 100 μg/L of BPA. Three female rats were used as controls. Placentas underwent histological examination and immunohistochemistry for von Willebr and factor (F-VIII) and caspase-9. Results: Sixty-seven fetuses have been produced, 30 from control rats and 37 from exposed rats. Exposed fetuses showed a lower longitudinal/transverse diameter ratio than controls (2.57 ± 0.29 vs. 2.78 ± 0.38, p < 0.05). Also, exposed fetuses showed a significant reduction in the number of placental vessels per field (124.86 ± 19.15 vs. 143.54 ± 22.09, p < 0.05). On the other hand, apoptosis is not increased by exposure, as shown by caspase-9 levels. Conclusion: Exposure to BPA during pregnancy may affect placental vascularization, and this phenomenon may explain the lower birth weight reported. However, our results do not show the increase in apoptosis observed in vitro.