RESUMEN
Obesity, considered a metabolic disorder, is one of the most significant health issues that the community has to cope with today. A rising number of studies have been conducted to find out promising genetic targets for obese treatment. The sympathetic nervous system was proven to possess remarkable roles in energy metabolism, including the stimulation of lipolysis as well as thermogenesis, via distinct adrenoceptors appearing on the membrane of adipocyte. A decrease of ß-adrenoceptor expression has been observed in obese individuals, which is related to reducing energy expenditure and developing obesity. While that the deficiency of stearoyl-CoA desaturase-1 (SCD1), which is a promising target for treatments of metabolic diseases, decreases oxidation and promotes the synthesis of fatty acids. Here, we emphasized several differences between distinct adrenoceptor subtypes, including their mRNA expression level and function in white adipose tissue and brown adipose tissue. We also highlighted SCD1's roles related to the progression of adipocytes and its changing expression under the obese condition in both rodents and humans, and furthermore, tried to figure out the interaction between adrenoceptors and SCD1 in adipose tissue.
Asunto(s)
Tejido Adiposo , Obesidad , Receptores Adrenérgicos , Estearoil-CoA Desaturasa , Humanos , Adipocitos/metabolismo , Tejido Adiposo/metabolismo , Adiposidad , Obesidad/metabolismo , Receptores Adrenérgicos/metabolismo , Estearoil-CoA Desaturasa/genética , Estearoil-CoA Desaturasa/metabolismoRESUMEN
Ear mesenchymal stem cells (EMSCs) have been investigated to differentiate into adipocytes, chondrocytes, and muscle cells in vitro. However, the factors controlling adipogenesis of this stem cell population in vitro, function, and type of adipocytes raised from them are still unclear. Here we found that genetics have a modest effect on adipogenic capacity of EMSCs. Adipocytes differentiated from EMSCs have a potential function in lipid metabolism as indicated by expression of lipogenic genes and this function of EMSC adipocytes is regulated by genetics. EMSCs failed to be differentiated into brite/brown adipocytes due to their lack of a thermogenic program, but adipocytes raised from EMSCs showed a fate of white adipocytes. Overall, our data suggest that EMSCs differentiate into functional white adipocytes in vitro and this is genetic-dependent.