High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS
High-fat diets exaggerate endocrine and metabolic phenotypes in a rat model of DHEA-induced PCOS
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高脂肪饮食夸大了 DHEA 诱导的 PCOS 大鼠模型的内分泌和代谢表型
DOI：
10.1530/rep-15-0542
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发表时间：
2016-04-01
期刊：
影响因子：
3.8
通讯作者：
Qiao, Jie
中科院分区：
文献类型：
--
作者：
Zhang, Haolin;Yi, Ming;Qiao, Jie
多囊卵巢综合征（PCOS）是一种病因不明、治疗不佳的复杂内分泌代谢疾病。饮食对多囊卵巢综合征表型的影响尚不完全清楚。在本研究中，我们采用45%和60%的高脂肪饮食（HFDs）治疗产后DHEA注射诱导的PCOS大鼠模型。我们发现DHEA和DHEA + HFDs大鼠均表现出生殖异常，包括高雄激素、不规则周期和多囊卵巢。添加HFDs，尤其是60%的HFDs，会加剧卵巢的形态变化和一些代谢变化，包括体重和体脂含量增加、葡萄糖耐量降低和血清胰岛素水平升高。qPCR结果显示，dhea诱导的下丘脑雄激素受体和LH受体的表达升高在添加60%的HFDs后被逆转。相比之下，卵巢LH受体和胰岛素受体mRNA的表达仅在添加60%的HFDs时上调。这些结果表明，DHEA和DHEA + HFDs可能通过不同的机制影响PCOS表型：DHEA通过LH影响下丘脑-垂体-卵巢轴的正常功能，而添加HFDs通过卵巢对胰岛素相关机制的反应加剧内分泌和代谢功能障碍。我们的结论是，添加HFDs可以产生dhea诱导的PCOS的不同表型，并且可以用于该综合征的生殖和代谢特征的研究。
Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder with unclear etiology and unsatisfactory management. Effects of diets on the phenotype of PCOS were not fully understood. In the present study, we applied 45 and 60% high-fat diets (HFDs) on a rat model of PCOS induced by postnatal DHEA injection. We found that both DHEA and DHEA + HFDs rats exhibited reproductive abnormalities, including hyperandrogenism, irregular cycles and polycystic ovaries. The addition of HFDs, especially 60% HFDs, exaggerated morphological changes of ovaries and a number of metabolic changes, including increased body weight and body fat content, impaired glucose tolerance and increased serum insulin levels. Results from qPCR showed that DHEA-induced increased expression of hypothalamic androgen receptor and LH receptor were reversed by the addition of 60% HFDs. In contrast, the ovarian expression of LH receptor and insulin receptor mRNA was upregulated only with the addition of 60% HFDs. These findings indicated that DHEA and DHEA + HFDs might influence PCOS phenotypes through distinct mechanisms: DHEA affects the normal function of hypothalamus-pituitary-ovarian axis through LH, whereas the addition of HFDs exaggerated endocrine and metabolic dysfunction through ovarian responses to insulin-related mechanisms. We concluded that the addition of HFDs yielded distinct phenotypes of DHEA-induced PCOS and could be used for studies on both reproductive and metabolic features of the syndrome.