中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2011年
4期
246-250
,共5页
茅原申%刘毅东%平萍%孙凯%吴旻%叶惟靖
茅原申%劉毅東%平萍%孫凱%吳旻%葉惟靖
모원신%류의동%평평%손개%오민%협유정
高脂饮食%睾丸%肥胖
高脂飲食%睪汍%肥胖
고지음식%고환%비반
High-fat diet%Testis%Obesity
目的 研究高脂饮食对青春期雄性Sprague Dawley大鼠睾丸发育过程的影响，并探究该影响是否具有可逆性。方法 将1月龄Sprague Dawley雄性大鼠60只，应用随机数字表法分为对照组（n=10）和营养性肥胖模型组(n=50)，分别用普通饲料和高脂饲料喂养8周后，将10只营养性肥胖模型组大鼠和对照组大鼠处死。采用酶联免疫法检测血清睾酮和雌二醇水平，HE染色观察左侧睾丸的组织学改变，Johnsen评分评价睾丸的生精能力。剩余40只大鼠应用随机数字表法分为高脂饮食组(n=13)、正常饮食组(n=13)和减肥组(n=14)，后两组大鼠均用普通饲料喂养，高脂饮食组大鼠用高脂饲料喂养，减肥组大鼠在正常饮食的基础上，每日跑步20 min，喂养6周后处死大鼠进行上述睾丸结构和功能研究。结果 高脂饮食8周后，营养性肥胖大鼠的体重明显高于对照组(O=0.006)。营养性肥胖大鼠的血清睾酮水平明显低于对照组(P=0.024)，血清雌二醇水平明显高于对照组(P =0.017)。HE染色显示：与对照组比较营养性肥胖大鼠曲精小管细胞层数减少，部分曲精小管萎缩。营养性肥胖大鼠的Johnsen评分明显低于对照组(P=0.000)。高脂饮食组的睾酮水平明显低于正常饮食组(P=0.001)和减肥组(P=0.000)，正常饮食组的睾酮水平也明显低于减肥组(P=0.001)。高脂饮食组的雌二醇水平明显高于正常饮食组(P=0.001)和减肥组（P=0.000），正常饮食组的雌二醇水平也明显高于减肥组(P=0.001)。HE染色显示：高脂饮食组和正常饮食组大鼠睾丸组织的病变无进行性加重；减肥组大鼠睾丸组织的病变较轻。减肥组的Johnsen评分均明显高于其他两组（P=0.000及0.001）。相关性分析显示，Johnsen评分与大鼠体重呈负相关（r=-0.962,P=0.000）；与血清睾酮水平呈正相关(r=0.916，P=0.000)。结论 高脂饮食能导致青春期雄性Sprague Dawley大鼠营养性肥胖。营养性肥胖大鼠表现为睾丸发育不全，生精功能减弱，内分泌功能障碍，运动减肥后以上改变有所改善。肥胖程度与生精功能呈负相关。
目的 研究高脂飲食對青春期雄性Sprague Dawley大鼠睪汍髮育過程的影響，併探究該影響是否具有可逆性。方法 將1月齡Sprague Dawley雄性大鼠60隻，應用隨機數字錶法分為對照組（n=10）和營養性肥胖模型組(n=50)，分彆用普通飼料和高脂飼料餵養8週後，將10隻營養性肥胖模型組大鼠和對照組大鼠處死。採用酶聯免疫法檢測血清睪酮和雌二醇水平，HE染色觀察左側睪汍的組織學改變，Johnsen評分評價睪汍的生精能力。剩餘40隻大鼠應用隨機數字錶法分為高脂飲食組(n=13)、正常飲食組(n=13)和減肥組(n=14)，後兩組大鼠均用普通飼料餵養，高脂飲食組大鼠用高脂飼料餵養，減肥組大鼠在正常飲食的基礎上，每日跑步20 min，餵養6週後處死大鼠進行上述睪汍結構和功能研究。結果 高脂飲食8週後，營養性肥胖大鼠的體重明顯高于對照組(O=0.006)。營養性肥胖大鼠的血清睪酮水平明顯低于對照組(P=0.024)，血清雌二醇水平明顯高于對照組(P =0.017)。HE染色顯示：與對照組比較營養性肥胖大鼠麯精小管細胞層數減少，部分麯精小管萎縮。營養性肥胖大鼠的Johnsen評分明顯低于對照組(P=0.000)。高脂飲食組的睪酮水平明顯低于正常飲食組(P=0.001)和減肥組(P=0.000)，正常飲食組的睪酮水平也明顯低于減肥組(P=0.001)。高脂飲食組的雌二醇水平明顯高于正常飲食組(P=0.001)和減肥組（P=0.000），正常飲食組的雌二醇水平也明顯高于減肥組(P=0.001)。HE染色顯示：高脂飲食組和正常飲食組大鼠睪汍組織的病變無進行性加重；減肥組大鼠睪汍組織的病變較輕。減肥組的Johnsen評分均明顯高于其他兩組（P=0.000及0.001）。相關性分析顯示，Johnsen評分與大鼠體重呈負相關（r=-0.962,P=0.000）；與血清睪酮水平呈正相關(r=0.916，P=0.000)。結論 高脂飲食能導緻青春期雄性Sprague Dawley大鼠營養性肥胖。營養性肥胖大鼠錶現為睪汍髮育不全，生精功能減弱，內分泌功能障礙，運動減肥後以上改變有所改善。肥胖程度與生精功能呈負相關。
목적 연구고지음식대청춘기웅성Sprague Dawley대서고환발육과정적영향，병탐구해영향시부구유가역성。방법 장1월령Sprague Dawley웅성대서60지，응용수궤수자표법분위대조조（n=10）화영양성비반모형조(n=50)，분별용보통사료화고지사료위양8주후，장10지영양성비반모형조대서화대조조대서처사。채용매련면역법검측혈청고동화자이순수평，HE염색관찰좌측고환적조직학개변，Johnsen평분평개고환적생정능력。잉여40지대서응용수궤수자표법분위고지음식조(n=13)、정상음식조(n=13)화감비조(n=14)，후량조대서균용보통사료위양，고지음식조대서용고지사료위양，감비조대서재정상음식적기출상，매일포보20 min，위양6주후처사대서진행상술고환결구화공능연구。결과 고지음식8주후，영양성비반대서적체중명현고우대조조(O=0.006)。영양성비반대서적혈청고동수평명현저우대조조(P=0.024)，혈청자이순수평명현고우대조조(P =0.017)。HE염색현시：여대조조비교영양성비반대서곡정소관세포층수감소，부분곡정소관위축。영양성비반대서적Johnsen평분명현저우대조조(P=0.000)。고지음식조적고동수평명현저우정상음식조(P=0.001)화감비조(P=0.000)，정상음식조적고동수평야명현저우감비조(P=0.001)。고지음식조적자이순수평명현고우정상음식조(P=0.001)화감비조（P=0.000），정상음식조적자이순수평야명현고우감비조(P=0.001)。HE염색현시：고지음식조화정상음식조대서고환조직적병변무진행성가중；감비조대서고환조직적병변교경。감비조적Johnsen평분균명현고우기타량조（P=0.000급0.001）。상관성분석현시，Johnsen평분여대서체중정부상관（r=-0.962,P=0.000）；여혈청고동수평정정상관(r=0.916，P=0.000)。결론 고지음식능도치청춘기웅성Sprague Dawley대서영양성비반。영양성비반대서표현위고환발육불전，생정공능감약，내분비공능장애，운동감비후이상개변유소개선。비반정도여생정공능정부상관。
Objective To investigate the effects of diet-induced obesity on the developmental process of testes in pubertal Sprague Dawley (SD) rats and explore the possible reversibility. Methods Sixty one-month-old male SD rats were randomly divided into a control group ( n =10) and a model group ( n =50 ), which were fed on a normal diet and a high-fat diet, respectively. After 8 weeks, all the rats in the control group and 10 rats randomly picked out from the model group were killed. The serum testosterone and estradiol levels were measured by enzymelinked inununosorbent assay. Their left testes sections were stained by HE method, and the histology was observed under optical microscope and the spermatogenic activity was evaluated by Johnsen scoring system. The remaining 40 rats in the model group were further randomly divided into 3 subgroups: continued high-fat diet subgroup ( n =13), resume normal diet subgroup (n =13), and weight-loss subgroup (n =14). The continued high-fat diet subgroup was fed by high-fat diet, while the other two subgroups were fed by normal diet. Rats in weight-loss group took normal diet with running 20 min/d. After 6 weeks, the same parameters were assessed using the same methods. Results After 8 weeks, compared with the control group, the testosterone level of the model group significantly decreased (P =0.024) and the estradiol level significantly increased ( P =0. 017). The result of HE staining showed that the spermatogenic cell layers decreased, with part of seminiferous tubule experiencing atrophy.The number of Leydig cell also decreased and lipo vacuole was seen in the interstitial tissue of testis. The Johnsen score of the model group was significantly lower than that of the control group (P =0.000). The testosterone level was significantly lower in the continued high-fat diet subgroup than that in resume normal diet subgroup ( P =0.001 ) and weight-loss subgroup ( P =0.000), and was significantly lower in resume normal diet subgroup than that in weight-loss subgroup ( P =0.001 ). The estradiol level was significantly higher in continued high-fat diet subgroup than that in resume normal diet subgroup ( P =0.001 ) and weight-loss group ( P =0.000 ), and was significantly higher in resume normal diet subgroup than that in weight-loss group ( P =0.001 ). HE staining showed that, pathological changes aggravating and worsening compared with the control group, the model group had significantly decreased seminiferous tubule cell layers, with some seminiferous tubules experiencing atrophy.The Johnsen score was significantly higher in weight-loss subgroup than that in the other two subgroups ( P =0.000and 0.001, respectively). The Johnsen score was negatively correlated with body weight ( r =- 0.962, P =0.000), and positively correhted with the serum testosterone level ( r =0.916, P =0.000 ). Conclusions High-fat diet can induce pubertal obesity in male SD rats, which is featured by testicular hypoplasia, decreased spermatogenesis, and endocrine dysfunction. Physical exercise may improve the conditions. The degree of obesity may be negatively correlated with the spermatogenic function.
