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肥胖症的早期发作会导致雌性大鼠的生殖缺陷。

Early onset of obesity induces reproductive deficits in female rats.

机构信息

Centro de Ciências Biológicas e da Saúde, Universidade Estadual do Oeste do Paraná (UNIOESTE), Cascavel, PR, Brazil.

出版信息

Physiol Behav. 2012 Mar 20;105(5):1104-11. doi: 10.1016/j.physbeh.2011.12.002. Epub 2011 Dec 11.

DOI:10.1016/j.physbeh.2011.12.002
PMID:22178647
Abstract

The incidence of obesity is increasing rapidly all over the world and results in numerous health detriments, including disruptions in reproduction. However, the mechanisms by which excess body fat interferes with reproductive functions are still not fully understood. After weaning, female rats were treated with a cafeteria diet or a chow diet (control group). Biometric and metabolic parameters were evaluated in adulthood. Reproductive parameters, including estradiol, progesterone, LH and prolactin during the proestrus afternoon, sexual behavior, ovulation rates and histological analysis of ovaries were also evaluated. Cafeteria diet was able to induce obesity in female rats by increasing body and fat pad weight, which resulted in increased levels of triglycerides, total cholesterol, LDL and induced insulin resistance. The cafeteria diet also negatively affected female reproduction by reducing the number of oocytes and preantral follicles, as well as the thickness of the follicular layer. Obese females did not show preovulatory progesterone and LH surges, though plasma estradiol and prolactin showed preovulatory surges similar to control rats. Nevertheless, sexual receptiveness was not altered by cafeteria diet. Taken together, our results suggest that the cafeteria diet administered from weaning age was able to induce obesity and reduce the reproductive capability in adult female rats, indicating that this obesity model can be used to better understand the mechanisms underlying reproductive dysfunction in obese subjects.

摘要

肥胖的发病率在全球范围内迅速上升,导致许多健康损害,包括生殖障碍。然而,过量脂肪如何干扰生殖功能的机制仍不完全清楚。断奶后,雌性大鼠接受 cafeteria 饮食或标准饮食(对照组)治疗。成年后评估生物计量和代谢参数。还评估了发情前期下午的雌二醇、孕酮、LH 和催乳素等生殖参数、性行为、排卵率以及卵巢的组织学分析。 cafeteria 饮食通过增加体重和脂肪垫重量使雌性大鼠产生肥胖,导致甘油三酯、总胆固醇、LDL 增加,并引起胰岛素抵抗。cafeteria 饮食还通过减少卵母细胞和窦前卵泡数量以及卵泡层厚度对雌性生殖产生负面影响。肥胖雌性大鼠虽然表现出类似对照大鼠的发情前雌二醇和催乳素激增,但没有出现排卵前孕酮和 LH 激增。然而,发情接受性不受 cafeteria 饮食的影响。总之,我们的结果表明,从断奶期开始给予 cafeteria 饮食能够诱导肥胖并降低成年雌性大鼠的生殖能力,表明这种肥胖模型可用于更好地理解肥胖人群生殖功能障碍的机制。

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