A Short S-Equol Exposure Has a Long-Term Inhibitory Effect on Adipogenesis in Mouse 3T3-L1 Cells

Applied Sciences

Carlos Galaviz-Hernández¹  Gilberto Mandujano-Lázaro²  Laurence A. Marchat²  César A. Reyes-López³  Fengyang Huang⁴  Abraham Giacoman-Martínez⁵  Julio C. Almanza-Pérez⁵  César López-Camarillo⁶ 

[1] Academia de Genómica, CIIDIR-Durango, Instituto Politécnico Nacional, Durango 34220, Mexico;Laboratorio 2 de Biomedicina Molecular, ENMH, Instituto Politécnico Nacional, Ciudad de México 07320, Mexico;Laboratorio de Bioquímica Estructural, ENMH, Instituto Politécnico Nacional, Ciudad de México 07320, Mexico;Laboratorio de Farmacología y Toxicología, Hospital Infantil de México Federico Gómez, Ciudad de México 06720, Mexico;Laboratorio de Farmacología, Departamento de Ciencias de la Salud, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, Ciudad de México 09340, Mexico;Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México 03100, Mexico;

关键词: 3T3-L1 cells;    adipogenesis;    adipokines;    estrogen receptor beta agonists;    S-equol;   

DOI  :  10.3390/app11209657

来源: DOAJ

【 摘 要 】

In the search for new drugs against obesity, the chronic disease that threatens human health worldwide, several works have focused on the study of estrogen homologs because of the role of estrogen receptors (ERs) in adipocyte growth. The isoflavone equol, an ERβ agonist, has shown beneficial metabolic effects in in vivo and in vitro assays; however, additional studies are required to better characterize its potential for body weight control. Here, we showed that the treatment of 3T3-L1 cells with 10 μM of S-equol for the first three days of the adipocyte differentiation protocol was able to prevent cells becoming semi-rounded and having a lipid droplet formation until the seventh day of culture; moreover, lipid accumulation was reduced by about 50%. Congruently, S-equol induced a reduction in mRNA expression of the adipogenic markers C/EBPα and PPARγ, and adipokines secretion, mainly Adiponectin, Leptin, Resistin, and MCP-1, while the release of PAI-1 was augmented. Moreover, it also reduced the expression of ERα and attenuated the subexpression of ERβ associated with adipogenesis. Altogether, our data suggested that S-equol binding to ERβ affects the transcriptional program that regulates adipogenesis and alters adipocyte functions. Future efforts will focus on studying the impact of S-equol on ER signaling pathways.

【 授权许可】

Unknown