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Obesity is one of the most invaliding and preventable diseases in the United States. Growing evidence suggests that there are sex differences in obesity in human and experimental animals. However, the specific mechanisms of this disease are unknown. Consequently, there is any particular treatment according to the sex/gender at this time. During the last decade, we observe a rise in the study of adipocyte and the possible mechanisms involved in the different roles of the fat. Furthermore, the effect of sex steroids on the adipocyte is one of the fields that need elucidation. Supporting evidence suggests that sex steroids play an essential role not only in the fat distribution, but also, in its metabolism, proliferation, and function. Thus, using in vitro and in vivo studies will contribute to our fight against this critical health public problem encompassing both sexes. In the present review, we discuss some of the recent advances in the adipocytes and the effect of the sex steroids on the adipose tissue. Also, we propose a new alternative to study the role of sex steroids on adipocyte biology through human adipose-derived stem cells.

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While three‐dimensional spheroids outperform traditional two‐dimensional monolayer culture for human adipose‐derived stem cells (hASCs), there is not a consensus on the most successful method for enhancing their adipogenic differentiation and minimizing the loss of physiologically relevant, fatty spheroids during culture. To this end, we compared three culture methods, namely, elastin‐like polypeptide‐polyethyleneimine (ELP‐PEI) coated surfaces, ultra‐low attachment static culture, and suspension culture for their ability to form and retain productive hASC spheroids. The ELP‐PEI coatings used the ELP conjugated to two molecular weights of PEI (800 or 25,000 g/mol). FTIR spectroscopy, atomic force microscopy, and contact angle goniometry revealed that the ELP‐PEI coatings had similar chemical structures, surface topography, and hydrophobicity. Time‐lapse microscopy showed that increasing the PEI molecular weight resulted in smaller spheroids. Measurement of triglyceride content showed that the three methods induced comparable differentiation of hASCs toward the adipogenic lineage. DNA content and morphometric analysis revealed merging of spheroids to form larger spheroids in the ultra‐low attachment static culture and suspension culture methods. In contrast, the retention of hASC spheroid sizes and numbers with a regular spheroid size (~100 μm) were best atop the ELP‐PEI800 coatings. Overall, this research shows that the spheroid culture atop the ELP‐PEI coatings is a suitable cell culture model for future studies involving long‐term, three‐dimensional culture of mature adipocytes derived from hASCs.

The Reduced Uterine Perfusion Pressure (RUPP) rat model and normal pregnant (NP) rat recipients of RUPP CD4+T cells recapitulate many characteristics of preeclampsia (PE) such as hypertension and oxidative stress. We have shown an important hypertensive role for NK cells to cause mitochondrial (mt) dysfunction in RUPP rats, however the role for RUPP CD4+ T cells to stimulate NK cells is unknown. Therefore, we hypothesize that RUPP induced CD4+ T cells activate NK cells to cause mt dysfunction/ROS as mechanisms of hypertension during pregnancy. We tested our hypothesis by adoptive transfer of RUPP CD4+T cells into NP rats or by inhibiting the activation of RUPP CD4+T cells with Orencia (Abatacept) and examining hypertension, NK cells and mt function. RUPP was performed on gestation day 14, splenic CD4+ T cells were isolated on GD19 and injected into NP rats on gestation day (GD) 13. In a separate groups of rats; Orencia was infused and the RUPP procedure performed. MAP and placental and renal mtROS increased in RUPP (n=7, p<0.05) and NP+RUPP CD4+ T cell recipients (n=13, p<0.05) compared to control NP (n=7) and NP+NPCD4+Tcell recipients (n=5), but was reduced with Orencia (n=13, p<0.05). Placental and renal respiration was reduced in RUPP (n=6, p<0.05) and NP+RUPP CD4+ T cells (n=6, state 3-p<0.05) compared to NP (n=5) and NP+NPCD4+Tcell recipients (n=5), but improved with Orencia (n=9, n=8 p<0.05). These data indicate that CD4+ T cells, independent of NK cells, cause mt dysfunction/ROS contributing to hypertension in response to placental ischemia during pregnancy.