Hrupka Brian J, Smith Gerard P, Geary Nori
Department of Psychiatry, Joan and Sanford I. Weill Medical College of Cornell University, New York, College of Cornell, New York, NY, USA.
Physiol Behav. 2002 Nov;77(2-3):233-41. doi: 10.1016/s0031-9384(02)00857-0.
To investigate further the site where estradiol (E(2)) inhibits food intake, we tested the effects on feeding of subcutaneous and intrahypothalamic implants of 10% E(2) benzoate in cholesterol (CHOL) or CHOL alone. E(2) was implanted subcutaneously in Silastic tubes, and intrahypothalamically via bilateral 29-gauge cannulas into the paraventricular nucleus (PVN) or the medial preoptic area (MPA) of ovariectomized (OVX) Sprague-Dawley and Long-Evans rats. Three-day implant periods followed 3-day baseline periods. Rats were allowed ad libitum access to chow and tap water, and food intake and body weight were measured each day. Subcutaneous 10% E(2) implants in Sprague-Dawley rats reduced food intake 21% on Day 2 and 34% on Day 3 (P's<.01) and decreased 3-day body weight gain 11 g (P<.05). In contrast, 10% E(2) implants in the PVN of Sprague-Dawley rats did not change food intake or body weight. Implants of 10% or 20% E(2) in the MPA also failed to decrease food intake. MPA implants of 10% E(2) decreased body weight gain 8 g (P<.05), but MPA implants of 20% E(2) decreased weight gain only 4 g (P>.05). To determine whether the strain of rat affected our negative results on food intake, we implanted 10% E(2) into the PVN of Long-Evans rats. Again, PVN E(2) did not decrease food intake significantly in comparison to the pretest baseline. PVN E(2) did, however, decrease body weight gain 5 g and decreased food intake 6% compared to rats with implants of CHOL (both P<.05), but these effects appeared to be due to an increase in feeding in the CHOL group in comparison to their baseline. Finally, CHOL and E(2) implants did not impair the responsivity of the PVN because acute implants of norepinephrine (NE) into the PVN of E(2)- or CHOL-treated Long-Evans rats significantly increased food intake. Our results do not support the hypothesis that E(2)'s actions in either the PVN or the MPA are sufficient to account for its inhibitory effects on feeding.
为了进一步研究雌二醇（E₂）抑制食物摄入的部位，我们测试了皮下和下丘脑内植入胆固醇（CHOL）中10% E₂苯甲酸盐或仅植入CHOL对进食的影响。将E₂皮下植入硅橡胶管中，并通过双侧29号套管下丘脑内注射到去卵巢（OVX）的Sprague-Dawley和Long-Evans大鼠的室旁核（PVN）或内侧视前区（MPA）。在3天的基线期后进行3天的植入期。大鼠可自由获取食物和自来水，每天测量食物摄入量和体重。Sprague-Dawley大鼠皮下植入10% E₂在第2天食物摄入量减少21%，第3天减少34%（P值<0.01），3天体重增加减少11克（P<0.05）。相比之下，Sprague-Dawley大鼠PVN内植入10% E₂并未改变食物摄入量或体重。MPA内植入10%或20% E₂也未能减少食物摄入量。MPA植入10% E₂使体重增加减少8克（P<0.05），但MPA植入20% E₂仅使体重增加减少4克（P>0.05）。为了确定大鼠品系是否影响我们在食物摄入方面的阴性结果，我们将10% E₂植入Long-Evans大鼠的PVN。同样，与测试前基线相比，PVN内植入E₂并未显著减少食物摄入量。然而，与植入CHOL的大鼠相比，PVN内植入E₂使体重增加减少了5克，食物摄入量减少了6%（两者P<0.05），但这些影响似乎是由于CHOL组与基线相比进食增加所致。最后，CHOL和E₂植入并未损害PVN的反应性，因为向接受E₂或CHOL处理的Long-Evans大鼠的PVN急性植入去甲肾上腺素（NE）会显著增加食物摄入量。我们的结果不支持E₂在PVN或MPA中的作用足以解释其对进食的抑制作用这一假设。
