Zhang Yunbo, Na Xiaolin, Zhang Yang, Li Lina, Zhao Xinyu, Cui Hongbin
Department of Food Nutrition and Hygiene, Public Health College, Harbin Medical University, Harbin, China.
Ann Nutr Metab. 2009;54(3):163-70. doi: 10.1159/000217812. Epub 2009 May 6.
BACKGROUND/AIMS: The primary objective of this study was to further determine the mechanisms by which isoflavone prevents obesity induced by ovariectomy.
Female 8-week-old Wistar rats were randomly assigned to 6 groups: a sham-operated group; an ovariectomized (OVX) control group; 3 OVX groups orally administered 400 ppm (L-SI), 1,200 ppm (M-SI) and 3,600 ppm (H-SI) of an isoflavone preparation, respectively, and an OVX group receiving 0.45 ppm of diethylstilbestrol. All animals were allowed free access to a high-fat diet and water for 4 weeks. Some neuropeptides, including ghrelin, neuropeptide Y (NPY), alpha-melanocyte-stimulating hormone (alpha-MSH), cholecystokinin (CCK), peptide YY (PYY), insulin and estradiol (E2), were measured by radioimmunoassay.
Compared with the OVX control group, body weight, total abdominal fat, food intake and food availability of the M-SI and H-SI groups were significantly reduced. The results also showed that isoflavone and diethylstilbestrol could decrease ghrelin and NPY levels and increase CCK, PYY and E2 levels. The level of alpha-MSH was not changed.
These findings showed that isoflavone could reduce obesity by decreasing food intake, possibly by (1) reducing ghrelin and NPY levels, thereby decreasing food intake, and (2) increasing CCK and PYY levels, which can induce satiety by irritating the vagal center.
背景/目的:本研究的主要目的是进一步确定异黄酮预防卵巢切除诱导的肥胖的机制。
将8周龄雌性Wistar大鼠随机分为6组:假手术组;卵巢切除(OVX)对照组;3个OVX组分别口服400 ppm(低剂量异黄酮,L-SI)、1200 ppm(中剂量异黄酮,M-SI)和3600 ppm(高剂量异黄酮,H-SI)的异黄酮制剂,以及1个接受0.45 ppm己烯雌酚的OVX组。所有动物自由摄取高脂饮食和水4周。采用放射免疫分析法检测一些神经肽,包括胃饥饿素、神经肽Y(NPY)、α-黑素细胞刺激素(α-MSH)、胆囊收缩素(CCK)、肽YY(PYY)、胰岛素和雌二醇(E2)。
与OVX对照组相比,M-SI组和H-SI组的体重、腹部总脂肪、食物摄入量和食物利用率均显著降低。结果还显示,异黄酮和己烯雌酚可降低胃饥饿素和NPY水平,提高CCK、PYY和E2水平。α-MSH水平未发生变化。
这些研究结果表明,异黄酮可能通过以下方式减少食物摄入量从而减轻肥胖:(1)降低胃饥饿素和NPY水平,从而减少食物摄入量;(2)提高CCK和PYY水平,通过刺激迷走神经中枢诱导饱腹感。