Ethanol decreases the expression of pituitary adenylate cyclase activating polypeptide in rat testes

The present study was designed to evaluate the effect of ethanol on pituitary adenylate cyclase activating polypeptide (PACAP) expression in adult rat testes. Ethanol (3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Using northern blot analysis, we elucidated the decrease of PACAP mRNA in rat testes by ethanol administration. The level of PACAP mRNA was decreased by 46.5% in testes of the ethanol-treated animals, compared to that of saline-treated animals. In particular, ethanol exposure decreased the expression of PACAP mRNA and protein in developing germ cells, which are sperm cell progenitors. Thus, our findings suggest that the decrease of PACAP in developing germ cells by ethanol administration may contribute to the suppression of male reproductive activity.     

Decrease of pituitary adenylate cyclase activating polypeptide and its type I receptor mRNAs in rat testes by ethanol exposure

The present study was designed to evaluate the effect of ethanol on pituitary adenylate cyclase activating polypeptide (PACAP) and its typ I (PAC1) receptor expression in adult rat testes. Ethanol (3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Using northern blot analysis, the present study showed the reduction of PACAP mRNA levels in rat testes by ethanol administration. Also, ethanol decreased the expression level of PAC1 receptor in testes. In particular, in situ hybridization clearly showed the decrease of PAC1 receptor mRNA expression in Leydig cells, which produce testosterone. Furthermore, the serum level of testosterone was significantly decreased in the ethanol-treated group. In conclusion, our findings suggest that the decrease of PACAP and PAC1 receptor expression in rat testes by ethanol exposure may partly contribute to the suppression of male reproductive activity.     

Ethanol exposure suppresses survival kinases activation in adult rat testes

The present study was designed to evaluate whether ethanol suppresses survival-signaling pathways in rat testes. Ethanol (1.5 g/kg or 3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Ethanol treatment significantly increased the number of TUNEL-positive cells in rat testes. Potential activation was measured by phosphorylation of Akt and Erk1/2 using Western blot analysis. Ethanol decreased the levels of activated survival kinases, pAkt and pErk1/2. The phosphorylation of Bad at Ser112 and Ser136 was decreased in ethanol-treated animals in comparison to saline-treated animals. Moreover, the interaction of pBad with 14-3-3 was decreased by ethanol exposure. In conclusion, our findings suggest that ethanol induces apoptotic cell death by suppressing the activation of survival kinases and the phosphorylation of their downstream targets in rat testes.     

Effects of 17beta-estradiol and tamoxifen on the selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) mRNA expression in male reproductive organs of rats

The selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) is highly expressed in testes under gonadotropin control. The expression patterns of PHGPx mRNA by 17beta-estradiol (E2) as an estrogen and tamoxifen (Tam) as an estrogen antagonist were investigated in the reproductive organs of male rats. Twelve-week-old male Sprague-Dawley rats were subcutaneously injected with E2 (7.5 microg/kg/day) or Tam (5 mg/kg/day) for 1 week. The E2 treatment significantly increased the levels of PHGPx mRNA in both testes and prostates, whereas the Tam treatment significantly decreased the levels of PHGPx mRNA, compared to the vehicle control (p<0.01). The treatment with E2 or Tam slightly decreased the levels of PHGPx mRNA in epididymides. In histopathological examination, severe vacuolization and depletion of germ cells in the seminiferous tubules, cell debris in the tubular lumen, and mild proliferative changes in interstitial tissues were observed in the testes of Tam-treated rats, whereas only mild spermatogonial proliferation was observed in the seminiferous tubules of E2-treated rats. There were no typical histopathological changes in the epididymides of any of the laboratory rats but mild epithelial proliferation in the prostates of E2- and Tam-treated rats. These results suggest that PHGPx mRNA expression may be influenced by estrogen in the male reproductive organs.     

炔雌醚暴露对幼年小鼠睾丸发育及增殖细胞核抗原、半胱氨酸蛋白酶-3表达的影响

This experiment was aimed to study the effect of quinestrol on the expression of PCNA and Caspase-3 in spermatogenic cells of juvenile mice. 4-week old male mice were randomly divided into four groups. Mice in the control group were injected intraperitoneally with olive oil alone and mice in the experiment groups were injected intraperitoneally with octylphenol resolved in olive oil at 1, 10, 100 mg/kg doses respectively for 1 week (once a day). The testes were immediately removed for weighing and serial cross-sections that were used for histological examination when the mice were 8-week-old. The expressions of PCNA and Caspase-3 in spermatogenic cells were determined by immunohistochemical method. The results showed that the thickness of the convoluted seminiferous tubule decreased, cellular deranged, cell layers decreased and intercellular space increased. Meanwhile, there were a large number of abnormal shedding of spermatocytes and round spermatids, but few elongated spermatids and spermatozoa. The expression of PCNA extremely significantly decreased and the expression of Caspase-3 extremely significantly increased as quinestrol dose increased (P＜0.01). Quinestrol caused male reproductive function injury through inhibiting proliferation and promoting apoptosis in spermatogenic cells by regulating the expression of associated proteins.     

Testicular morphology and cauda epididymal sperm reserves of male rats exposed to Nigerian Qua Iboe Brent crude oil

Potential negative effects of exposure to Nigerian Qua Iboe Brent crude oil on the reproductive system of male rats was investigated. Forty Sprague-Dawley rats were used for the experiment. Exposure to Nigerian Qua Iboe Brent crude oil was achieved via oral administration of increasing doses (0.1, 0.2, and 0.4 ml/rat) every other day for 4 weeks. Cauda epididymal sperm reserves and relative weights of the testes as well as histological features of the testes of rats that received the crude oil treatment were compared to those of control rats. The results described here showed a significant (p < 0.01) dose-dependent reduction in the cauda epididymal sperm reserves of rats that received crude oil treatment relative to the control group. The morphology of testes of the crude oil-exposed rats was characterized by the presence of interstitial exudates, degeneration, and necrosis of spermatogenic and interstitial (Leydig) cells. Findings indicate that exposure of male rats to Nigerian Qua Iboe Brent crude oil may have adversely affected their reproductive systems. This may imply possible reproductive health hazards for animals and humans that may be exposed to this environmental pollutant, especially in areas where oil spillage is a common feature.     

Streptozotocin-induced diabetes increases apoptosis through JNK phosphorylation and Bax activation in rat testes

Diabetic disease is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway. Diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg) and testis samples were collected after 3 months. Compared with controls, body weight and testicular weight were lower in the diabetic group, and the apoptotic index in testicular germ cells was significantly increased. Expression of phospho-JNK and Bax was significantly increased in the diabetic group, and the level of activated caspase-3 was also increased, compared to that of controls. Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in rat testes through phosphorylation of JNK and activation of Bax.     

利用家蚕蛹生物反应器生产的人粒细胞/巨噬细胞集落刺激因子口服给药的临床前安全性评价

开发了用家蚕蛹表达的人粒细胞-巨噬细胞集落刺激因子(rhGM-CSF)的口服药物。试验评价了猕猴、大鼠和小鼠口服rhGM-CSF毒性情况,包括遗传毒性、单剂量和重复剂量的全身毒性以及生殖毒性。毒理学试验显示:静脉给药在NIH小鼠中最大耐受剂量为3 300μg/kg,LD50为2 020μg/kg,在SD大鼠中LD50为3 660μg/kg。在猕猴和大鼠的重复剂量毒性试验结果中显示:口服rhGM-CSF后,除了雌性SD大鼠的血糖含量外,其余各项指标包括白细胞、红细胞、血红蛋白含量、血小板数量以及血细胞凝集等都正常。雌性大鼠每天口服剂量为1 250μg/kg时,给药后血糖浓度显著增加(P<0.001),但在恢复期间可恢复到正常水平。微核实验、CHL染色体畸变试验和埃姆斯测验法都表明无论是在体内还是体外服用rhGM-CSF均未见遗传毒性,普通的生殖毒性试验和围产期及致畸敏感期的毒性试验均未见异常现象,表明口服rhGM-CSF无明显生殖毒性。临床前毒性试验表明口服超过临床剂量10倍的rhGM-CSF与严重的慢性中毒没有联系,其在药理学有效剂量的范围内是很安全的。     

Curcumin mitigates fenthion-induced testicular toxicity in rats: histopathological and immunohistochemical study

Fenthion is a widely used organophosphorus pesticide in agriculture that induces different cytotoxic effects, including male reproductive toxicity. The present work aimed to study the ameliorative effects of curcumin, a potential therapeutic agent against several chronic diseases, on reproductive toxicity induced by the organophosphate insecticide fenthion. Forty adult male albino rats were divided into four groups. The control group received distilled water. The curcumin group was administered curcumin at a dose of 100 mg kg^?1 body weight. The fenthion group was administered fenthion at a dose of 0.001 mg kg^?1. The fenthion/curcumin group was administered fenthion and curcumin together at the same doses. After four weeks of daily oral administration, the animals were sacrificed and their testes were excised. Specimens were processed for histopatholological and immunohistochemical investigations. Light and electron microscopic analysis visualised dramatic degenerative changes in seminiferous tubules as indicated by atrophy, necrosis, vacuolation and decreased number of spermatogenic cells. Moreover, the fenthion group showed a significant reduction in the proliferating cell nuclear antigen (PCNA)-immunoreactivity. Decreased PCNA-immunoreactivity reflected the depletion in the proliferation rate of spermatogenic cells and suggesting arrested spermatogenesis. Curcumin administration to fenthion-treated rats revealed mild degenerative changes with partial improvement of active spermatogenesis. In conclusion, these data may confirm the cytoprotective potency of curcumin against fenthion-induced cyto-toxicity.     

The Effects of Dietary l-Carnitine Supplementation on Semen Traits,Reproductive Parameters,and Testicular Histology of Japanese Quail Breeders

The present study was conducted to determine the effects of supplemental dietary l-carnitine at different levels on semen traits, reproductive parameters, and testicular histology in male Japanese quail breeders. Forty-five 5-wk-old male Japanese quail breeders were fed the same basal diet that was supplemented with 0 (control), 250, or 500 mg of l-carnitine/kg of diet. There were no significant effects of dietary l-carnitine supplementation at different levels on BW, feed intake, testes weight, fertility rate, hatchability rate of set and fertile eggs, and malonaldehyde production (μg/mL of semen) of male Japanese quail breeders. However, the supplementation of dietary l-carnitine at levels of 250 or 500 mg/kg to a basal diet significantly increased sperm viability and decreased multinucleated giant cells per testes in mature male Japanese quail breeders. Additional studies are required to explore the antioxidant role that l-carnitine has in Japanese quail breeders.     

Decreased sperm number and motile activity on the F1 offspring maternally exposed to butyl p-hydroxybenzoic acid (butyl paraben)

Butyl p-hydroxybenzoic acid (butyl paraben, BP) is widely used as a preservative in food and cosmetic products. Routledge et al showed that BP is weakly estrogenic in both in vitro and in vivo (rat uterotrophic) analyses. We investigated whether maternal exposures to BP during gestation and lactation periods affected the development of the reproductive organs of the F1 offspring. Pregnant Sprague-Dawley rats were injected subcutaneously with 100 or 200 mg/kg of BP from gestation day (GD) 6 to postnatal day (PND) 20. In the group exposed to 200 mg/kg of BP, the proportion of pups born alive and the proportion of pups surviving to weaning were decreased. The body weights of female offspring were significantly decreased at PND 49. The weights of testes, seminal vesicles and prostate glands were significantly decreased in rats exposed to 100 mg/kg of BP on PND 49. In contrast, the weights of female reproductive organs were not affected by BP. The sperm count and the sperm motile activity in the epididymis were significantly decreased at doses of 100 and 200 mg/kg of BP. In accordance with the sperm count in the epididymis, the number of round spermatids and elongated spermatids in the seminiferous tubule (stage VII) were significantly decreased by BP. Testicular expression of estrogen receptor (ER)-alpha and ER-beta mRNA was significantly increased in 200 mg/kg of BP treated group at PND 90. Taken together, these results indicated that maternal exposure of BP might have adverse effects on the F1 male offspring.     

Effect of Cadmium on Lipid Peroxidation and on Some Antioxidants in the Liver,Kidneys and Testes of Rats Given Diet Containing Cadmium-polluted Radish Bulbs

The aim of this study was to examine the effects of cadmium (Cd), incorporated in radish bulbs, on malondialdehyde and glutathione levels and on superoxide dismutase activity in the liver, kidneys and testes of male rats. The control animals were given diet containing ordinary radish bulbs for 4, 8 and 12 weeks, while contaminated animals were given diet containing Cd-polluted radish bulbs (1.1 mg Cd/g of diet) for the same periods as in the controls. At each time point, rats were euthanized and the liver, kidneys and testes were removed. The results indicated that the body weight gain of contaminated rats was identical to that of the control rats. Cd concentrations in the liver, kidneys and testes increased significantly and gradually from the 4th to 12th week of treatment. Malondialdehyde concentrations decreased significantly in the liver and increased significantly in the kidneys and testes after 12 weeks of treatment, while glutathione levels increased significantly in the liver, and decreased significantly in the kidneys and testes at the same time. No changes were observed in SOD activity in the liver, while in the kidneys and testes, this activity was increased after 12 weeks of treatment as compared with the control rats.     

2-Bromopropane induced germ cell apoptosis during spermatogenesis in male rat

2-Bromopropane (2-BP) causes testicular toxicity in humans and rats. However, the germ cell degeneration of testicular toxicity by 2-BP has not been understood. 2-BP at doses of 135, 405, and 1,355 mg/kg/day was daily injected subcutaneously into Sprague-Dawley rats for 28 days. At the dose of 1,355 mg/kg/day, 2-BP significantly decreased the weights of body and testes, eipididymis, seminal vesicle, and prostate, as well as daily sperm production. Atrophy of seminiferous tubules accompanied with degeneration of germ cells such as spermatogonia, spermatocytes, and elongated spermatids was observed in the testes of rats exposed to the 405 mg/kg/day and 1,355 mg/kg/day of 2-BP. TUNEL-positive germ cells were appeared in the 405 and 1,355 mg/kg/day of 2-BP-treated groups. In addition, ultrastructure alterations of apoptotic germ cells were observed by the electron microscopy study. Dead elongated spermatids were observed at 1,355 mg/kg/day after 28 days exposure. These results suggest that 2-BP impair spermatogenesis may result from apoptotic germ cell death.     

Effects of antiepileptic drugs carbamazepine and sodium valproate on fertility of male rats

The effects of carbamazepine and sodium valproate on fertility of male rats were studied. The tested drugs were given orally to male rats for 30 and 60 consecutive days. Mating performance, sex organs weights, semen quality, plasma concentrations of sexual hormones as well as histopathological findings were the criteria used to evaluate the reproductive efficiency of treated males. Oral administration of carbamazepine and sodium valproate for 30 and 60 consecutive days significantly decreased the testicular weight, sperm cell concentration, live sperms and percentage of progressively motile spermatozoa. Both drugs significantly increased the percentage of morphologically abnormal spermatozoa. A decrease in plasma testosterone, FSH and LH and an increase in prolactin levels were observed in the treated groups. Histopathological examination showed mild to moderate degenerative changes in the testes of the treated rats while the prostate glands and seminal vesicles appeared normal. A recovery period of 30 days was accompanied by marked changes in the tested parameters towards initial values.     

Thirteen-weeks subcutaneous treatment with high dose of natural sex hormones in rats with special reference to their effect on the pituitary-gonadal axis. I. Oestradiol

A high dose of oestradiol (0.3 mg/kg/day) was administrated subcutaneously to male and female rats daily for 13 weeks. The effects of hormonal treatment on various parameters were studied. The results revealed that treatment with oestradiol resulted in alopecia, retarded hair regrowth, decreased body weight and food consumption and reduced Hb, PCV and total RBCs. Neutrophilic leucocytosis, elevated ESR, and decreased blood glucose levels were also observed. Atrophy of the ovaries, testes and secondary sex organs was also recorded. The uterus of the oestradiol treated rats displayed endometrial epithelial cell hyperplasia and hypertrophy of the myometrium. The pituitary gland of the rats with oestradiol had a significant increase in the number of PRL and ACTH cells together with cytological criteria indicative of increased secretory activity; the gonadotropin-producing cells showed involutionary changes. The mammary glands of the oestradiol treated rats showed maximal stromal and ductal proliferation and minimal acinar proliferation.     

Testicular alterations in cryptorchid/orchiopexic rats chronically exposed to acrylamide or di-butyl-phthalate

Exposure of Sprague-Dawley (SD) rats to acrylamide (AA) or di-butyl-phthalate (DBP) from the 12th gestational day to the 16th postnatal week (PNW) has been shown to reduce the effectiveness of orchiopexy in recovering the testicular alterations associated with experimental cryptorchidism established at weaning. Herein, we provide information about the long-term effects of AA or DBP on the testes of cryptorchid/orchiopexic rats. Male offspring exposed in utero to 10 mg/kg/day AA or 500 mg/kg/day DBP underwent bilateral surgical cryptorchidism at the 3rd PNW and orchiopexy at the 6th week, with continuous exposure to the chemicals through diet until the 58th week. Regardless of the test chemical, there were severe qualitative/quantitative alterations in the seminiferous tubules and increased numbers of Leydig cells. There was an increase and decrease in the number of tubules with c-Kit- and placental alkaline phosphatase-labeled germ cells, respectively, as compared to those in the control group, suggesting an imbalance between apoptosis and cell proliferation processes. The histological scores of the testicular lesions at the end of this one-year study were higher than those in the previous 16-week study, indicating that exposure of rats to the toxicants AA or DBP enhanced the testicular alterations induced by the chemicals beginning at the intra-uterine life, and impaired the effectiveness of orchiopexy in restoring the testes to normal morphology. Although the present experimental protocol does not completely replicate the natural human undescended testes, our findings may contribute to understanding the alterations occurring in cryptorchid/orchiopexic testes potentially exposed to exogenous chemicals for extended periods.     

Exposure to 3-methyl-4-nitrophenol affects testicular morphology and induces spermatogenic cell apoptosis in immature male rats

The pollutant 3-methyl-4-nitrophenol (PNMC), a major component of diesel exhaust particles, can cause many adverse health problems. In the present study, we investigated the effects of PNMC on the testes of Sprague Dawley rats treated subcutaneously for 5 days with different doses of PNMC (1, 10 or 100 mg/kg). Exposure to PNMC caused a significant decrease in the plasma testosterone levels and in the absolute and relative weights of the testes. Severe histological lesions were observed in the testes of PNMC-treated animals. The ratio of the epithelial height to the seminiferous tubule diameter increased markedly in the PNMC-treated rats compared with the corresponding controls. In addition, PNMC exposure significantly increased the number of apoptotic spermatogenic cells compared with the controls whereas a significant decrease in the ratios of Bcl-2/Bax was observed at the same doses. These results suggest that PNMC exerts its gonadotoxicity in the rat mainly via apoptosis.     

Detection of in vivo DNA damage induced by ethanol in multiple organs of pregnant mice using the alkaline single cell gel electrophoresis (Comet) assay

Ethanol is principal ingredient of alcohol beverage, but considered as human carcinogen, and has neurotoxicity. Alcohol consumption during pregnancy often causes fetal alcohol syndrome. The DNA damage is one of the important factors in carcinogenicity or teratogenicity. To detect the DNA damage induced by ethanol, we used an in vivo alkaline single cell gel electrophoresis (Comet) assay in pregnant mice organs and embryos. Pregnant ICR mice on Day 7 of gestation were treated with 2, 4 or 8 g/kg ethanol, and maternal organs/tissues and embryos were subjected to the Comet assay at 4, 8, 12 and 24 hr after ethanol treatment. Four and 8 g/kg ethanol induced DNA damage in brain, lung and embryos at 4 or 8 hr after the treatment. Two g/kg ethanol did not cause any DNA damage, and 8 g/kg ethanol only increased the duration of DNA damage without distinct increase in the degree of the damage. No significant DNA damage was observed in the liver. To detect the effect of acetaldehyde, disulfiram, acetaldehyde dehydrogenase inhibitor, was administered before 4 g/kg ethanol treatment. No significant increase of DNA damage was observed in the disulfiram pre-treated group. These data indicate that ethanol induces DNA damage, which might be related to ethanol toxicity. Since pre-treatment of disulfiram did not increase DNA damage, DNA damage observed in this study might not be the effect of acetaldehyde.     

Reduction of carbon tetrachloride-induced hepatotoxic effects by oral administration of betaine in male Han-Wistar rats: a morphometric histological study

Eighty-five male Han-Wistar rats were arranged into three groups: CCl4-exposed rats, CCl4 + betaine-exposed rats, and control rats. To see the effect of betaine alone, five rats of the control and of the CCl4 + betaine groups were sacrificed after 7 days, before exposure to CCl4. After that, two of the groups (the CCl4 and CCl4 + betaine groups) were exposed to CCl4 (1 ml/kg per day subcutaneously [SC] for 4 consecutive days), and one of the groups (control group) was given olive oil (1 ml/kg per day SC for 4 consecutive days). At the start of the study (day 0), day 1, day 2, day 3, day 4, and 3 days after the last CCl4 and olive oil injections (day 7), samples of five rats per group were sacrificed, and the livers were taken for chemical analyses and histological examination. Oral betaine, after the acclimation period of a week, increased the number of mitochondria but not mitochondria size (day 0), compared with the case in control rats. Exposure to CCl4 resulted in centrilobular hepatic steatosis, and the administration of betaine significantly reduced this. Morphometric analyses also revealed that the addition of betaine increased the volume density of rough endoplasmic reticulum (RER) in the perinuclear areas of liver cell cytoplasm (day 7). Additionally, the administration of betaine prevented the reduction of Golgi complexes and mitochondrial figures in the cytoplasm observed after the exposures to CCl4. Also, the volume density of mitochondria was smallest in the CCl4-group, but the difference was not statistically significant. The results indicate that oral betaine either improves recovery or reduces the toxic effects of CCl4 on cell organelles in liver cells of male Han-Wistar rats.     

促性腺激素抑制激素对SD大鼠性腺生殖功能与糖代谢的影响

【目的】 探究促性腺激素抑制激素（GnIH）对SD大鼠性腺生殖功能和糖代谢的影响,以及SD大鼠性腺生殖功能和糖代谢之间的相关性。【方法】 将36只SD大鼠随机均分为对照组（0.9％生理盐水）、1 μg/100 μL GnIH组（Ⅰ组）、10 μg/100 μL GnIH （Ⅱ组）,每组12只（雌雄各半）。每天07：00和19：00注射生理盐水或GnIH （200 μL/次）,连续注射14 d后测量大鼠体重,计算肥胖程度,麻醉处死后采集卵巢和睾丸,称重并计算卵体比和睾体比;运用阴道涂片法观察雌性大鼠发情周期的变化;显微镜下观察并计算雄性大鼠精子活力;HE染色观察卵巢和睾丸组织变化;用实时荧光定量PCR法检测卵巢和睾丸中糖代谢基因胰岛素受体（IR）、葡萄糖转运蛋白4（GLUT4）和炎症相关因子肿瘤坏死因子（TNF-α）、白介素1β（IL-1β）的表达水平,并用SPSS 22.0软件分析生殖功能和糖代谢之间的相关性。【结果】 与对照组相比,Ⅰ组雌性SD大鼠和Ⅱ组雄性SD大鼠肥胖程度均显著升高（P<0.05）;Ⅱ组卵巢大小/重量、卵体比显著升高,睾丸重量、睾体比显著下降（P<0.05）。HE染色结果显示,与对照组相比,Ⅱ组雌性大鼠卵泡呈囊性扩张,颗粒细胞层减少,卵泡腔变大;Ⅰ、Ⅱ组雄性大鼠的生精小管均出现空泡样改变,生精细胞排列紊乱、层次减少。与对照组相比,Ⅱ组大鼠发情前期的持续时间显著延长（P<0.05）、精子活力显著下降（P<0.05）。实时荧光定量PCR结果显示,与对照组相比,Ⅰ、Ⅱ组雌性大鼠GLUT4基因的表达量极显著下降（P<0.01）、Ⅱ组中IR基因的表达量显著降低（P<0.05）,Ⅰ、Ⅱ组雄性大鼠GLUT4基因的表达量均极显著降低（P<0.01）;Ⅰ组雌性大鼠TNF-α、IL-1β基因和雄性大鼠IL-1β基因的表达量均显著升高（P<0.05）,Ⅱ组雌、雄大鼠TNF-α基因的表达量均极显著升高（P<0.01）。相关性分析结果显示,腹腔注射GnIH后,雌性大鼠的卵体比与GLUT4基因表达水平呈极显著正相关（P<0.01）,与IR基因的表达水平呈显著正相关（P<0.05）;雌性大鼠的发情周期与GLUT4基因表达水平呈极显著负相关（P<0.01）;雄性大鼠睾体比与GLUT4基因表达水平均呈显著正相关（P<0.05）,而精子活力与GLUT4基因表达水平均呈极显著正相关（P<0.01）。【结论】 腹腔注射GnIH能够抑制大鼠的生殖功能和导致糖代谢功能紊乱,而且GnIH可能参与性腺能量代谢与生殖功能的交叉对话,是能量代谢与生殖功能的新型联络因子。