Resistance of male Sprague-Dawley rats to sucrose-induced obesity: effects of 18-methoxycoronaridine.
Resistance of male Sprague-Dawley rats to sucrose-induced obesity: effects of 18-methoxycoronaridine.
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DOI：
10.1016/j.physbeh.2010.10.010
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发表时间：
2011-02-01
影响因子：
2.9
通讯作者：
Glick SD
中科院分区：
文献类型：
--
作者：
Taraschenko OD;Maisonneuve IM;Glick SD
有证据表明，男性和女性肥胖的发展可能是由不同的机制介导的，从而避免了不同的治疗方法。在本实验室的先前研究中，高蔗糖饮食诱导雌性Sprague-Dawley大鼠体重过度增加，给予α3β4烟碱受体的选择性拮抗剂18-甲氧基冠孢定（18-MC）可预防这种形式的肥胖。在本研究中，通过使用相同的实验方案，在雄性大鼠中研究了相似的参数。本研究亦评估重复给予18-MC对雄性大鼠体重增加、脂肪沉积、消费行为及肥胖生化指标的影响。与雌性动物相反，雄性动物自由采食蔗糖溶液（30%）并结合正常食物不会变得肥胖;它们没有过度增重，也没有过度脂肪沉积。重复给药18-MC（20 mg/kg，i. p.）在不改变食物或液体摄入的情况下，消耗蔗糖的动物和对照动物的体重增加均减弱。目前的研究结果表明，男性和女性是不同的反应高碳水化合物饮食肥胖。这种性别差异可能是次要的性别特异性改变胆碱能机制的喂养和体重调节。
Evidence suggests that the development of obesity in males and females might be mediated by distinct mechanisms, warranting different treatment approaches. In previous studies from this laboratory, a high sucrose diet induced excessive weight gain in female Sprague-Dawley rats and administration of a selective antagonist of α3β4 nicotinic receptors, 18-methoxycoronaridine (18-MC), prevented this form of obesity. In the present study similar parameters were studied in male rats by using an identical experimental protocol. The effects of repeated administration of 18-MC on body weight gain, deposition of fat, consummatory behavior and biochemical markers of obesity in male rats were also assessed. In contrast to females, males consuming ad libitum quantities of sucrose solution (30%) in combination with normal chow did not become obese; they did not gain excessive weight nor show excessive fat deposition. Repeated administration of 18-MC (20 mg/kg, i.p.) attenuated weight gain in both sucrose-consuming and control animals without altering food or fluid intake. The present results indicate that males and females are differentially responsive to high carbohydrate-diet obesity. Such gender disparities could be secondary to sex-specific alterations in cholinergic mechanisms of feeding and body weight regulation.