Research On The Effects Of Estrogen On Sweentness Signal Transduction In STC-1Cell

In this study, the mouse intestinal endocrine cell line STC-1was used for the study, which was the most commonly research tool for taste The changes in intracellular Ca2+release and extracellular ATP concentration were detected when17β-estradiol (E2) and sweeteners (sucrose, AK) were administrated to the STC-1cells. The mRNA expressions of estrogen receptors (ERα, ERβ and GPER) and sweet key signaling molecules (T1R2/T1R3, Ga, PLCβ2and TRPM5) were monitored by qRT-PCR. Moreover, the sweet signaling proteins (T1R2/T1R3,Ga, PLCβ2and TRPM5) were tested by Western blotting analysis. This study was aimed to investigate the mechanism underlying the effects of estrogen on the sweetness signal transduction, providing more inportant information for better understanding the changed sweetness perception by estrogen, as well as the related feeding behavior and obesity. The main findings were as follows.The intracellular Ca2+level was increased with the increasing sucrose concentration. Meawhile, the extracellular level of ATP was increased with the increasing sweetner concentration. With the increasing sucrose concentration, the extracellular level of ATP was increased first with a reducing trend thereafter. In contrast, the extracellular level of ATP was increased first with a lasting high level thereafter with the increasing AK concentration. Pretreatment with a low concentration (1nM) of E2for12h had no effect on the sucrose-induced intracellular Ca2+release; wheras the physiological concentration10nM and a higher concentration50nM of E2was able to promote the intracellular Ca2+release significantly. In addition, lOnM E2promoted the release of extracellular ATP triggered by sucrose or AK. Pretreatment with different concentrations of E2for10min, much shorter than12h, only50nM E2was able to promote the sucrose-induced release of intracellular Ca2+and extracellular ATP.It was confirmed that the three subtypes of estrogen receptors, ERa, ERβ and GPER, were expressed in STC-1cells by qRT-PCR, with higher levels of ERa and GPER. Pretreatment with lOnM E2for12h upregulated the mRNA levels of T1R2and PLCP2significantly, which was able to promote the mRNA expressions of T1R2, T1R3, Ga and PLC02induced by sucrose, as well as the mRNA expression of Ga induced by AK. Further, Western blotting analysis showed that10nM E2promoted the protein expressions of T1R3, PLCβ2and TRPM5induced by sucrose. However, no significant impact on the protein expression of sweet taste signal transduction molecules induced by AK.Taken together, estrogen can influence the sweetness signal transduction via chronic genomic mechanisms mediated by estrogen receptors.