Abstract
BackgroundEstrogen was reported to protect against obesity, however the mechanism remains unclear. We aimed to investigate the impact of 17β-estradiol (17β-E2) on triglyceride metabolism in adipocytes with or without lipopolysacchride (LPS) stimulating, providing novel potential mechanism for estrogen action.Methods3T3-L1 adipocytes were cultured and differentiated into mature adipocytes in vitro. The differentiated 3T3-L1 cells were divided into six groups: (i) control group, treated with 0.1% DMSO alone; (ii) 17β-E2 group, treated with 1, 0.1, or 0.001 μM 17β-E2 for 48 h; (iii) 17β-E2 plus MPP group, pre-treated with 10 μM MPP (a selective ERα receptor inhibitor) for 1 h, then incubated with 1 μM 17β-E2 for 48 h; (iv) 17β-E2 plus PHTPP group, pre-treated with 10 μM PHTPP (a selective ERβ receptor inhibitor), then incubated with 1 μM 17β-E2 for 48 h; (v) LPS group, pre-treated with 100 ng/mL LPS for 24 h, then cells were washed by PBS for 3 times and incubated with 0.1% DMSO alone for 48 h; (vi) 17β-E2 plus LPS group, pre-treated with 100 ng/mL LPS for 24 h, then cells were washed by PBS for 3 times and incubated with 1 μM 17β-E2 for 48 h. The levels of triglyceride and adipose triglyceride lipase (ATGL) in differentiated 3T3-L1 cells and the concentrations of interleukin-6 (IL-6) in culture medium were measured.ResultsComparing with control group, 1 μM and 0.1 μM 17β-E2 decreased the intracellular TG levels by about 20% and 10% respectively (all P < 0.05). The triglyceride-lowing effect of 17β-E2 in differentiated 3T3-L1 cells was abolished by ERα antagonist MPP but not ERβ antagonist PHTPP. Comparing with control group, the IL-6 levels were significantly higher in the culture medium of the cultured differentiated 3T3-L1 cells in LPS group and 17β-E2 + LPS group (all P < 0.05). And, the IL-6 levels were similar in LPS group and 17β-E2 + LPS group (P > 0.05). There was no significant difference in the triglyceride contents of differentiated 3T3-L1 cells among control group, LPS group and 17β-E2 + LPS group (all P > 0.05). ATGL expression in 17β-E2 group was significantly higher than control group (P < 0.05), which was abolished by ERα antagonist MPP or LPS.Conclusions17β-E2 increased ATGL expression and lowered triglycerides in adipocytes but not in LPS stimulated adipocytes via estrogen ERα.
Highlights
Estrogen was reported to protect against obesity, the mechanism remains unclear
Cell culture and differentiation The 3T3-L1 cells were obtained from the American Type Culture Collection (ATCC, Rockville, USA) and cultured in Dulbecco modified eagle medium (DMEM, GIBICO, Invitrogen corporation, Changsha, china) supplemented with 10% fetal bovine serum
The triglyceride-lowing effect of 17β-E2 in differentiated 3T3-L1 cells was abolished by Estrogen receptor α (ERα) antagonist MPP, while Estrogen receptor β (ERβ) antagonist PHTPP did not significantly affect the TG-lowing effect (Fig. 2)
Summary
Estrogen was reported to protect against obesity, the mechanism remains unclear. Previous studies reported the prevalence of obesity and metabolic syndrome in menopausal women is 3.3-fold higher among postmenopausal women than premenopausal women. Donato et al reported postmenopausal women have five times the chance of having central adiposity than premenopausal women, even after controlling for BMI and other confounding factors [2]. Ovariectomy result in a significant weight gain and which can be reversed with the administration of exogenous estradiol [4,5,6]. This evidence indicates the rapid decline of estrogen levels contributes to obesity and estrogen can protect against obesity. The anti-obesity mechanism of estradiol is still unclear
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