Effect of 2-hydroxyestradiol on binge intake in rats.

Effect of 2-hydroxyestradiol on binge intake in rats.
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DOI:
10.1016/j.physbeh.2011.03.029
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发表时间:
2011-07-06
影响因子:
2.9
通讯作者:
Corwin, R. L. W.
Corwin, R. L. W.
中科院分区:
医学3区
文献类型:
--
作者:
Babbs, R. K.;Wojnicki, F. H. E.;Corwin, R. L. W.

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暴饮暴食的一个难题是,女性更有可能患有与暴饮暴食相关的疾病,尽管雌二醇会减少食物的摄入量。2-羟基雌二醇(2OHE2)是一种雌激素代谢产物,可能是这种矛盾的原因,因为它可能干扰DA信号。我们假设,在啮齿动物模型中,2OHE2会增强暴饮暴食。将34只非饥饿大鼠分为每日对照组(D组)和暴饮组(INT组),每组各1只(1男1女),D组每天摄入任意来源的脂肪20分钟,INT组每天间歇性摄入脂肪20分钟。在5周的暴饮暴食诱导期内,女性的缩短摄入量增加的速度明显快于男性,因此在5周后,男性每公斤体重摄入的脂肪明显少于女性。这一结果与生物差异导致暴饮暴食的性别差异的观点是一致的。然后大鼠在脂肪摄入之前立即注射2OHE2(1.0,3.0和10.0μg/kg)、赋形剂或2-甲氧基雌二醇(2ME2)。2OHE2只显著刺激INT大鼠的脂肪摄入量(p<0.03)。此外,这种影响在女性身上似乎比在男性身上更微妙。因此,2OHE2似乎会加剧暴饮暴食的规模。这些数据表明,饮食失调风险的性别差异存在一种新的生物学机制。
One conundrum of binge eating is that women are more likely to suffer from binge-related disorders, even though estradiol decreases food intake. 2-hydroxyestradiol (2OHE2), an estrogen metabolite, may account for the contradiction, due to possible interference with DA signaling. We hypothesized that 2OHE2 would enhance bingeing in a rodent model. Two cohorts (1 male, 1 female) of 34 non-food-deprived rats were separated into daily control (D) (received an optional source of dietary fat for 20 minutes every day) or bingeing (INT) groups (received fat intermittently, i.e. 20 minutes on Mon, Weds, Fri). During the 5-wk binge induction period, shortening intakes escalated significantly faster in females than in males, such that males consumed significantly less fat/kg body mass than did females after 5 weeks. This result is consistent with the idea that biological differences contribute to sex differences in bingeing. Rats were then injected with 2OHE2 (1.0, 3.0, and 10.0 μg/kg intraperitoneally), vehicle, or 2-methoxyestradiol (2ME2) immediately prior to fat access. Fat intake was significantly stimulated by 2OHE2 only in the INT rats (p<0.03). Furthermore, this effect seemed to be more subtle in females than in males. Thus, 2OHE2 appears to exacerbate binge size. These data suggest a novel biological mechanism for sex differences in the risk of eating disorders.
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