Objective:To investigate the effect of obesity on fertility in male rat,and preliminarily explore the mechanism of oxidative damage.Methods:The six-week-old SD male rats were randomly divided into the control(normal diet,n =15)and obese groups (high-fat diet,n =30).The body weight,organ indexes,serum metabolic parameters,reproductive hormones(GnRH,FSH,LH,total T,E2) and SHBG of two groups were assayed after feeding for 16 weeks.Indicators of reproductive function,including apoptosis of spermatogenic cells,oxidative stress,and sperm count and motility were determined.The differences between the two groups were compared.Results:Body weight and Lee index were significantly increased,and the level of leptin [(3.17±0.23)vs.(2.33±0.21) ng/ml],insulin [(28.99±2.43) vs.(20.62±1.72) μU/ml] and TG [(0.55±0.03) vs.(0.36±0.04) mmol/L] were significantly increased(P＜0.05),and GnRH [(36.46±1.95) vs.(45.51±2.75) pg/ml],LH [(3.06±0.37) vs.(4.67±0.70) U/L],T [(0.81±0.13) vs.(1.98±0.32) ng/ml],SHBG [(55.31±3.80) vs.(71.69±4.65) nmol/L] were significantly decreased(P＜0.05) in obese ratscompared with the control group.In addition,the apoptosis index [(4.26±0.35)％ vs.(3.09±0.28)％]of spermatogenic cells in testis was significantly increased in obese rats by TUNEL assay.The oxidativedamage with increased SOD and decreased MDA in obese rats was significantly different from that incontrol group(P＜0.05).Compared with the control group,sperm motility [(14.36±7.67) ％ vs.(36.40±9.17)％] was significantly decreased (P＜0.01),while the sperm concentration was not significantlydecreased(P＞0.05).Conclusions:Obesity induced by high-fat diet leads to decrease sperm motility in male rats,which maybe associated with metabolic and reproductive endocrine disorders,as well as apoptosis and oxidativedamage of testicular tissue.%目的 研究肥胖对雄性大鼠生殖功能的影响,初步探讨其氧化损伤的相关机制.方法 6周龄SD雄性大鼠随机分成对照组(普通饮食,15只)和肥胖组(高脂饮食,30只).喂养16周后,处死,测定体重、脏器系数、代谢参数和生殖内分泌激素(GnRH、FSH、LH、TT、E2)和SHBG,检测睾丸生精细胞凋亡、氧化应激和附睾精子参数,比较两组各指标差异.结果 与对照组大鼠相比,肥胖组大鼠体重和Lee指数明显增加,血清瘦素(Lep)[(3.17±0.23)ng/ml vs.(2.33±0.21)ng/m1]、胰岛素(INS)[(28.99±2.43)μU/ml vs.(20.62±1.72)μU/ml]和甘油三酯(TG)[(0.55±0.03)mmol/L vs.(0.36±0.04)mmol/L]显著升高,血清GnRH[(36.46±1.95)pg/ml vs.(45.51±2.75)pg/ml]、LH[(3.06±0.37)U/L vs.(4.67±0.70)U/L]、总睾酮(TT)[(0.81±0.13)ng/ml vs.(1.98±0.32)ng/ml]、SHBG[(55.31±3.80)nmol/L vs.(71.69±4.65)nmol/L]显著降低,差异均有统计学意义(P＜0.05);TUNEL结果显示,肥胖组大鼠睾丸生精细胞凋亡指数显著高于对照组[(4.26±0.35)％ vs.(3.09士0.28)％,P＜0.05];氧化应激结果表明,肥胖组大鼠的MDA上升、SOD降低,差异有统计学意义(P＜0.05);附睾精子分析发现,与对照组相比,肥胖组大鼠的精子活力显著下降[(14.36±7.67)％vs.(36.40±9.17)％,P＜0.01],而精子浓度无显著性差异(P＞0.05).结论 高脂饮食诱导雄性大鼠的肥胖,代谢和生殖内分泌紊乱,氧化损伤增加,导致生精细胞凋亡增加,并最终使精子活力下降.
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