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运动通过下调干细胞因子、上调胃饥饿素和使氧化应激正常化来预防肥胖诱导的精液异常。

Exercise protects against obesity induced semen abnormalities via downregulating stem cell factor, upregulating Ghrelin and normalizing oxidative stress.

作者信息

Alhashem Fahaid, Alkhateeb Mahmoud, Sakr Hussein, Alshahrani Mesfer, Alsunaidi Mohammad, Elrefaey Hesham, Alessa Riyad, Sarhan Mohammad, Eleawa Samy M, Khalil Mohammad A

机构信息

Department of Physiology, College of Medicine, King Khalid University, Abha, Kingdom of Saudi Arabia.

Department of Obstetrics and Gynecology, College of Medicine, King Khalid University, Abha, Kingdom of Saudi Arabia.

出版信息

EXCLI J. 2014 May 26;13:551-72. eCollection 2014.

Abstract

Increased oxidative stress and hormonal imbalance have been hypothesized to underlie infertility in obese animals. However, recent evidence suggests that Ghrelin and Stem Cell Factor (SCF) play an important role in fertility, in lean individuals. Therefore, this study aimed at investigating whether changes in the levels of Ghrelin and SCF in rat testes underlie semen abnormal parameters observed in obese rats, and secondly, whether endurance exercise or Orlistat can protect against changes in Ghrelin, SCF, and/or semen parameters in diet induced obese rats. Obesity was modelled in male Wistar rats using High Fat Diet (HFD) 12-week protocol. Eight week-old rats (n=40) were divided into four groups, namely, Group I: fed with a standard diet (12 % of calories as fat); Group II: fed HFD (40 % of calories as fat); Group III: fed the HFD with a concomitant dose of Orlistat (200 mg/kg); and Group IV: fed the HFD and underwent 30 min daily swimming exercise. The model was validated by measuring the levels of testosterone, FSH, LH, estradiol, leptin, triglycerides, total, HDL, and LDL cholesterol, and final change in body weight. Levels were consistent with published obesity models (see Results). As predicted, the HFD group had a 76.8 % decrease in sperm count, 44.72 % decrease in sperm motility, as well as 47.09 % increase in abnormal sperm morphology. Unlike the control group, in the HFD group (i.e. obese rats) Ghrelin mRNA and protein were elevated, while SCF mRNA and protein were diminished in the testes. Furthermore, in the HFD group, SOD and GPx activities were significantly reduced, 48.5±5.8 % (P=0.0012) and 45.6±4.6 % (P=0.0019), respectively, while TBARS levels were significantly increased (112.7±8.9 %, P=0.0001). Finally, endurance exercise training and Orlistat administration individually and differentially protected semen parameters in obese rats. The mechanism includes, but is not limited to, normalizing the levels of Ghrelin, SCF, SOD, GPx and TBARS. In rat testes, diet induced obesity down regulates SCF expression, upregulates Ghrelin expression, and deteriorate oxidative stress levels, which are collectively detrimental to semen parameters. Exercise, and to a lesser extent Orlistat administration, protected effectively against this detrimental effect.

摘要

氧化应激增加和激素失衡被认为是肥胖动物不育的潜在原因。然而,最近的证据表明,胃饥饿素和干细胞因子(SCF)在瘦个体的生育能力中起重要作用。因此,本研究旨在调查肥胖大鼠睾丸中胃饥饿素和SCF水平的变化是否是肥胖大鼠精液参数异常的原因,其次,耐力运动或奥利司他是否可以预防饮食诱导的肥胖大鼠中胃饥饿素、SCF和/或精液参数的变化。使用高脂饮食(HFD)12周方案在雄性Wistar大鼠中建立肥胖模型。将8周龄大鼠(n = 40)分为四组,即:第一组:喂食标准饮食(12%的热量来自脂肪);第二组:喂食HFD(40%的热量来自脂肪);第三组:喂食HFD并同时给予奥利司他(200 mg/kg);第四组:喂食HFD并每天进行30分钟游泳运动。通过测量睾酮、促卵泡激素(FSH)、促黄体生成素(LH)、雌二醇、瘦素、甘油三酯、总胆固醇、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)胆固醇水平以及体重的最终变化来验证该模型。这些水平与已发表的肥胖模型一致(见结果)。如预期的那样,HFD组的精子数量减少了76.8%,精子活力降低了44.72%,异常精子形态增加了47.09%。与对照组不同,在HFD组(即肥胖大鼠)中,睾丸中的胃饥饿素mRNA和蛋白升高,而SCF mRNA和蛋白减少。此外,在HFD组中,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)活性分别显著降低,为48.5±5.8%(P = 0.0012)和45.6±4.6%(P = 0.0019),而丙二醛(TBARS)水平显著升高(112.7±8.9%,P = 0.0001)。最后,耐力运动训练和奥利司他给药分别且不同程度地保护了肥胖大鼠的精液参数。其机制包括但不限于使胃饥饿素、SCF、SOD、GPx和TBARS水平正常化。在大鼠睾丸中,饮食诱导的肥胖下调SCF表达,上调胃饥饿素表达,并使氧化应激水平恶化,这些共同对精液参数有害。运动以及在较小程度上的奥利司他给药有效地预防了这种有害影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bec/4464503/fde19565b54e/EXCLI-13-551-t-001.jpg

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