维药罗补甫克比日丸对DM性勃起功能障碍大鼠性激素水平的影响

目的:揭示维药罗补甫克比日丸对糖尿病(DM)性勃起功能障碍(ED)大鼠性激素水平的影响。方法:取50只SD雄性大鼠,从中随机取7只设为正常对照(A)组,余43只行腹腔注射链尿佐菌素(STZ)制造DM动物模型,未成模者为STZ组,成模者用阿朴吗啡(APO)筛选DM性ED模型,并将其随机分为DM性ED对照组、药罗补甫克比日丸(C)组、胰岛素(D)组、联用(E)组,未成ED模者为DM(F)组,共7组。药物干预6周后,检测外周血中性激素水平。结果:正常对照(A)组、DM性ED胰岛素(D)组、DM性ED联用(E)组、STZ(G)组睾酮(T)水平显著高于DM性ED对照(B)组、DM性ED伊木萨克(C)组、DM(F)组,有显著性差异(P0.01);正常对照(A)组、STZ(G)组促黄体生成激素(LH)水平显著低于DM性ED伊木萨克(C)组、DM性ED联用(E)组,有显著性差异(P0.05、P0.01);DM性ED对照(B)组、DM性ED补甫克比日丸(C)组促卵泡刺激素(FSH)水平显著低于DM性ED胰岛素(D)组、DM性ED联用(E)组,有显著性差异(P0.01、P0.05)。结论:维药罗补甫克比日丸可显著改善DM性ED大鼠睾酮水平,且与胰岛素联用优于单用,维药罗补甫克比日丸治疗DM性ED的作用机制可能与T、LH、FSH含量变化有关。     

实时剪切波弹性定量分析不同睾酮水平大鼠阴茎组织硬度

目的:利用实时剪切波弹性成像(shear wave elastography,SWE)定量分析不同睾酮水平阴茎组织硬度之间的差异。方法:睾酮水平不同SD大鼠两组,低睾酮水平组(1月龄,睾酮水平1.00~1.50 ng/m L,n=10)和高睾酮水平组(13月龄,睾酮水平2.00~2.50ng/m L,n=10)。采用放射免疫法测定各组大鼠血清睾酮水平。选用法国Super Sonic Imagine公司生产的Aixplorer超声诊断仪,启动SWE模式对阴茎进行SWE成像并测量其剪切波硬度(shear wave stiffness,SWS)。分析比较两组大鼠血清睾酮水平之间的差异及SWS之间的差异。结果:所有大鼠血清睾酮水平及阴茎组织SWS的测量均成功完成。低睾酮水平组大鼠血清睾酮水平为(1.30±0.16)ng/m L,高睾酮水平组为(2.29±0.14)ng/m L,两组大鼠血清睾酮水平存在显著差异(P0.01);低睾酮水平组大鼠阴茎组织SWS为(9.86±0.72)k Pa,高睾酮水平组为(7.80±1.43)k Pa,两组大鼠阴茎组织SWS存在显著差异(P0.01)。结论:SWE可以检测出睾酮水平不同导致的阴茎组织硬度的差异,提示SWE可作为一项评价阴茎组织硬度的无创新技术。     

不同造模方法对大鼠多囊卵巢综合征模型的影响

目的采用不同方法诱导SD清洁级雌性大鼠多囊卵巢综合征(PCOS)动物模型,造模完成后检测大鼠血清相关激素并观察卵巢局部形态学改变,并探讨其意义。方法分别采用来曲唑、硫酸普拉睾酮钠、硫酸普拉睾酮钠联合HCG诱导大鼠PCO模型,RIA法测定血清LH、FSH、E2、P、T、PRL、INS水平,HE染色后光镜下观察卵巢局部形态。结果A组(对照组)和B组(来曲唑组)比较,B组较A组血清FSH浓度升高,血清P浓度降低,差异有统计学意义(P0.05);B组血清T浓度较A组明显升高,差异有显著统计学意义(P0.01)。D组(硫酸普拉睾酮钠组)与C组(对照组)比较,两组间血清性激素及INS差异无显著性(P0.05)。E组(硫酸普拉睾酮钠联合HCG组)与C组比较,E组血清T浓度、LH/FSH比值较C组升高,差异有统计学意义(P0.05)。E组与D组比较,血清P、T浓度升高,差异有统计学意义(P0.05)。A、C两组卵巢局部形态基本正常,可见发育成熟的卵泡及优势卵泡,B、D、E三组未见优势卵泡,均可见卵巢多囊样改变。结论使用来曲唑或硫酸普拉睾酮钠联合HCG诱导大鼠PCOS模型,无论在影响血清性激素还是卵巢局部形态学改变方面与临床表现很接近,符合动物PCOS造模要求。     

菊藤胶囊对应激性高血压大鼠血压及血液ET、NO含量的影响

目的:探讨了菊藤胶囊对应激性高血压(SIH)大鼠血压影响的可能机制。方法:采用电击足底应激刺激的方法制备应激性高血压大鼠模型,观察每天应激刺激前灌服菊藤胶囊对应激大鼠血压的影响,检测血清一氧化氮(NO)、血浆内皮素(ET)水平。结果:模型组血压显著升高,模型组与其它各组血压比较差异均有统计学意义(P<0.01)。正常组、卡托组、菊高组之间进行比较,差异无统计学意义(P>0.05);与模型组比较,菊藤胶囊高中剂量组、西药组可使SIH血清NO水平显著升高(P<0.01),高中剂量组、西药组可使血浆ET水平显著下降(P<0.01);正常组、西药组、中药高剂量组之间进行比较并无显著性差异。结论:SIH形成与血清NO水平下降、血浆ET水平升高有关,菊藤胶囊能有效降低血压,其降压机制可能与调整血清NO、血浆ET水平有关。     

GnRH-A主动免疫家兔的去势效果

为了探讨促性腺激素释放激素类似物(gonadotropin releasing hormone analogue,GnRH-A)对动物免疫去势的效果及作用机理.在30只日本大耳白兔(Oryctolagus cuniculus)(EG-Ⅰ与EG-Ⅱ组)的颈背部皮下分2.3点注射1.0ml(100/gml)自制的GnRH-A抗原乳剂,EG-Ⅱ组3周后加强免疫一次;测定睾丸长度与重量、体重、血清GnRH抗体效价及睾酮浓度.结果表明,EG-Ⅱ组睾丸长度与EG-I组差异极显著(P<0.01);EG-Ⅱ组的GnRH抗体水平明显高于EG-Ⅰ组;EG-Ⅱ组、EG-Ⅰ组与对照组的血清睾酮浓度差异逐渐增加,102 d时EG-Ⅱ组睾酮浓度极显著低于对照组(P<0.01),且第28 d后EG-Ⅱ组睾酮浓度显著低于EG-Ⅰ组(P<0.05);EG-Ⅱ组体重和日增重最大,显著高于EG-Ⅰ组及对照组(P<0.05).GnRH-A主动免疫家兔对睾丸发育、血清GnRH抗体效价和睾酮浓度具有显著的影响,加强免疫效果更理想.     

维药罗补甫克比日丸对DM 性ED 大鼠阴茎组织中NOS含量的影响

目的:揭示维药罗补甫克比日丸对糖尿病(DM)性勃起功能障碍(ED)大鼠阴茎组织中一氧化氮合酶(NOS)含量的影响。方法:取50只SD雄性大鼠,从中随机取7只设为正常对照(A)组,余43只行腹腔注射链尿佐菌素(STZ)制造DM动物模型,未成模者为STZ(G)组,成模者用阿朴吗啡(APO)筛选DM性ED模型,并将其随机分为DM性ED对照(B)组、罗补甫克比日丸(C)组、胰岛素(D)组、联用(E)组,未成ED模者为DM(F)组,共7组。药物干预6周后,检测阴茎组织中NOS含量及外周血中睾酮(T)水平,并显微镜下观察大鼠阴茎组织结构的变化。结果:正常对照(A)组、DM性ED胰岛素(D)组、DM性ED联用(E)组、STZ(G)组NOS、T水平显著高于DM性ED对照(B)组、DM性ED罗补甫克比日丸(C)组、DM(F)组,有显著性差异(P0.01);HE染色,正常对照(A)组、DM性ED胰岛素(D)组、DM性ED联用(E)组、STZ(G)组大鼠阴茎海绵体结构正常;DM性ED对照(B)组、DM性ED罗补甫克比日丸(C)组、DM(F)组阴茎平滑肌细胞数量减少,平滑肌细胞分布杂乱,内皮细胞明显破坏,胶原纤维大量增生,阴茎间质组织内微小血管管壁变厚,血管管腔不规则、狭窄或闭塞。结论:维药罗补甫克比日丸与胰岛素联用可显著改善DM性ED大鼠NOS、T水平。     

GnRH-a对大鼠海马和皮质部位parvalbumin表达的影响

目的:研究促性腺激素释放激素类似物(gonadotropin releasing hormone analogue,GnRH-a)对大鼠海马、皮质部位小白蛋白(parvalbumin,PV)表达的影响.方法:采用酶联免疫吸附试验测定血清激素水平,免疫组织化学和图像分析观察大鼠海马、皮质部位PV的表达.结果:①GnRH-a组大鼠血清雌二醇(estradiol,E2)、LH及FSH水平较正常对照组下降,差异有统计学意义(P<0.05);与OVX组比较LH、FSH较低,差异有统计学意义(P<0.05),但E2差异不显著.②正常情况下,大鼠海马、皮质部位可观察到PV神经元及纤维分布.③GnRH-a组PV细胞数及灰度值低于正常对照组,差异有统计学意义(P<0.05),与去卵巢组大鼠组相似;GnRH-a+E2联合用药后,PV细胞数及灰度值与正常对照组相似.结论:GnRH-a降低大鼠海马、皮质部位神经元中PV的表达,从而影响神经元的功能,这可能与其用药后神经精神副反应有一定关系.     

四川成都市郊正常成年男性血清生殖激素水平及其频数分布

本文用放射免疫测定法(RIA),测定了200～290例中国四川成都市郊30～73岁的正常成年男性血清睾酮(T)促黄体激素(LH).卵泡刺激素(FSH)及泌乳激素(PRL)的水平及其分布,进行了不同年龄水平差异显著性的观察,见到睾酮与泌乳激素水平无显著差异,促黄体激素及卵泡刺激素水平,随年龄之增加而升高,差异有显著性,并测得它们在血清中水平的分布:LH、FSH及PRL均为对数正态公布,T既非正态又非对数正态,但其频率分布较对称,接近正态分布。     

有氧运动与饮食控制对2型糖尿病大鼠肝chemerin及其受体CMKLR1的影响

目的：研究4周有氧运动与饮食控制对2型糖尿病（DM）大鼠肝chemerin及其受体趋化因子样受体1（CMKLR1）的影响及其在改善糖脂代谢中的影响。方法：50只雄性SD大鼠随机分为正常对照组（Con,n=6）和糖尿病造模组（n=44）。采用高脂高糖饲料联合小剂量链脲佐菌素（STZ）（30 mg/kg）的方法制备2型糖尿病模型大鼠。造模成功的DM大鼠随机分为4组（n=6）：糖尿病对照组（DM）、糖尿病运动组（EDM）、改喂普通饲料的糖尿病饮食控制组（NDM）和糖尿病运动+饮食控制组（ENDM）。运动组大鼠进行为期4周中等强度跑台有氧运动,每周运动6 d。采用罗氏血糖仪检测大鼠空腹血糖（FBG）,全自动生化分析仪检测大鼠血清总胆固醇（TC）、甘油三酯（TG）和低密度脂蛋白（LDL）水平,real time PCR和Western blot分别检测大鼠肝chemerin、CMKLR1的mRNA和蛋白水平。结果：DM大鼠FBG和血清TC、TG、LDL水平显著升高的同时,肝chemerin和CMKLR1的mRNA和蛋白水平显著增加;4周有氧运动和/或饮食控制显著降低EDM、NDM和ENDM组FBG和血清TC、TG、LDL的同时,显著降低这3组大鼠的肝chemerin蛋白水平,其中ENDM组降低最显著（P<0.01）;NDM和ENDM组大鼠的肝CMKLR1蛋白水平升高（P<0.01）。结论：4周有氧运动和/或饮食控制降低2型糖尿病大鼠的肝chemerin蛋白水平、增加CMKLR1蛋白水平,这可能与其改善糖尿病大鼠的糖脂代谢有关。     

多囊卵巢综合征患者血清HSP70、IMA水平的变化及与性激素和氧化应激的相关性研究

目的:探讨多囊卵巢综合征(PCOS)患者血清热休克蛋白70(HSP70)、缺血修饰白蛋白(IMA)水平的变化及与性激素指标和氧化应激指标的相关性。方法:选择2017年6月~2018年6月华中科技大学同济医学院附属同济医院收治的未经治疗的初诊PCOS患者87例为PCOS组,另随机选择同期在本院进行体检的健康育龄妇女87例为对照组,比较两组血清HSP70、IMA、性激素指标、氧化应激指标,分析血清HSP70、IMA水平与性激素、氧化应激的相关性。结果:PCOS组患者血清卵泡刺激素(FSH)、促黄体生成素(LH)、睾酮(T)、8-异前列腺素F2α(8-isoPGF2α)、丙二醛(MDA)、HSP70、IMA水平显著高于对照组,差异有统计学意义(P<0.05);PCOS组患者血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-Px)水平低于对照组,差异有统计学意义(P<0.05);PCOS组血清雌二醇(E2)、泌乳素(PRL)水平与对照组比较差异无统计学意义(P>0.05)。PCOS患者血清HSP70、IMA水平与血清FSH、LH、T、8-iso PGF2α、MDA水平呈正相关关系,与SOD、GSH-Px水平呈负相关关系(P<0.05),与E2、PRL水平无显著相关性(P>0.05)。结论:血清HSP70、IMA水平在PCOS患者呈现异常升高,其水平改变与性激素及氧化应激水平密切相关,提示HSP70、IMA可能参与了PCOS的病理过程,临床检测HSP70、IMA的水平变化有可能为PCOS诊疗提供有效的预测作用。     

Senescence and steroid hormone receptor reactivities in accessory sex glands of elderly rats (Sprague-Dawley) following exogenous hormonal therapy

The aim of this study was to characterize the stromal and epithelial distribution of AR, ERα and ERβ reactivities in the different accessory sex glands of elderly rats and during strong hormonal changes. Ten month old male rats were divided into six senile groups and submitted to treatment: Senile/Control group (SC); Senile/Testosterone group (ST): Senile/Estrogen group (SE); Castrated group (CA); Castrated/Testosterone group (CT); Castrated/Estrogen group (CE). After a 30-day treatment, the prostatic ventral lobe (VL), dorsal lobe (DL) and coagulating gland (CG) samples were processed for immunohistochemistry and Western Blotting. The results showed that AR immunoreactivity was characterized in the epithelium of VL and DL in senile/control rats and senile rats submitted to exogenous hormonal therapy. AR reactivity in the coagulating gland was verified predominantly in the stromal cells in the different experimental groups. ERα reactivity occurred predominantly in the stromal compartment in all accessory sex glands. In the DL and CG, ERα immunoreactivities were intense in the groups which received testosterone (ST) and estrogen (SE). ERβ immunoreactivity in the CG was verified in the stromal compartment in the different experimental groups, showing a positive response to both increased testosterone and estrogen levels. ERβ reactivity, in the DL, was intensified in the stroma of senile rats with higher serum testosterone levels, and in senile rats with increased serum estrogen levels, especially in the glandular epithelium. Thus, the results revealed different distribution pattern of steroid hormone receptors in each one of the prostatic lobes in senescence, especially in the prostate dorsal lobe and coagulating gland, which is a fundamental factor due to the fact that major prostatic diseases occur in a later period of life.     

Alteration in the normal pattern of serum testosterone and 5α-androstane-3α,17β-diol in the immature male rat following chronic treatment with luteinizing hormone releasing hormone or luteinizing hormone

A major component of sexual maturation in the male rat is a progressive decline in serum concentrations of 5α-androstane-3α,17β-diol (3α-diol) and a concomitant increase in testicular testosterone biosynthesis and secretion. Chronic administration of synthetic luteinizing hormone releasing hormone (LHRH) or luteinizing hormone (LH)/human chorionic gonadotropin (hCG) to immature male rats has been shown to result in a delay in sexual maturation as evidenced by decreased sex accessory gland weights and altered testicular testosterone production. We have examined the postulate that such treatments may either reverse or retard the normal developmental pattern of serum testosterone and 3α-diol concentrations. Chronic $\text{in vivo}$ treatment of 28 day old immature male rats for 2 weeks with daily injections of either 0.5 μg of LHRH, 1.0 μg of LHRH, or 30 μg of LH was found to result in significant reductions in weights of the seminal vesicles and ventral prostate glands and diminutions in serum testosterone concentrations. Serum content of 3α-diol was either unchanged or slightly elevated in the LHRH treated animals and increased significantly in the LH treated animals. These data suggest that either a reversal of or retardation in the normal developmental pattern of serum testosterone and 3α-diol content has been achieved in the immature male rat by chronic LHRH or LH treatment.     

Streptozotocin-induced type 1 diabetes mellitus alters the morphology, secretory function and acyl lipid contents in the isolated rat parotid salivary gland

Diabetes mellitus (DM) is associated with numerous conditions including hypo-secretion of digestive enzymes. This study investigated the morphology, secretory function (alpha-amylase release) and acyl lipid contents in the isolated parotid gland of STZ-induced diabetic and age-matched control rats in order to provide insights into diabetes-induced salivary insufficiency. The techniques employed included light microscopy, colourimetric and gas chromatography (GC) analysis, respectively. Diabetes mellitus was induced in adult male Wistar rats by a single intraperitoneal (IP) injection of streptozotocin (STZ) (60 mg per kg body weight). Control animals were injected with a similar volume of citrate buffer. The animals were tested for DM 4 days after STZ injection and 2 months later when they were humanely killed for the experiment. The morphological results showed diabetic parotid glands to be extensively infiltrated with lipid droplets of various magnitudes, whereas glands from control animals display normal structure with the absence of lipid droplets. The analysis of parotid secretory function revealed a significant (p < 0.05) dose-dependent decrease in alpha-amylase release in response to noradrenaline (NA) in STZ-treated glands when compared to age-match control parotid glands. Furthermore, the levels of acyl lipids (16:0, 16:1, 18:0 and 18:1) in diabetic parotid glands was significantly (p < 0.01) reduced compared to control glands, along with a reduced ratio of 16:1/16:0. The results indicate DM can elicit changes in the morphology, secretory function and acyl fatty acid quantity in the isolated rat parotid gland.     

Age-dependent changes in the concentration of active sex steroids,precursors, metabolites,and regulatory agents in blood serum of male subjects

We measured blood concentration of active and non-active sex steroids, metabolites, and precursors and compared to changes in protein and peptide hormones controlling the reproductive axis (total 14 hormones and hormone-like substances) in male subjects aged 18 to 72 y.o. We found a significant decrease in serum concentration of precursors for active sex steroids (pregnenolone, progesterone, dehydroepiandrosterone, and DHEA-sulfate), free testosterone, androstenedione (non-active metabolite of testosterone) as well as 5α-dihydrotestone after the age of 35. However, the level of total testosterone and estradiol (another active testosterone metabolite) remained steady. The systems regulated production of active sex steroids resisted a higher load associated with age and caused the increase in luteinizing and follicle-stimulating hormones in hypophysis and activin in steroidogenic glands directly correlating with age; negative correlation for these hormones was confirmed with certain sex steroids explaining the negative feedback. Decrease in level of hypopheseal adrenocorticotropic hormone with age demonstrated a more substantial role for adrenal glands compared to that of testicles in reduction of blood concentration of active sex steroids. In general, despite the reduced activity of steroidogenic glands in 60-to 70-year old male subjects the level of testosterone and estradiol remained unchanged due to associated growth of level of luteinizing and follicle-stimulating hypopheseal hormones as well as activin in steroidogenic glands that stimulated biosynthesis of sex steroids. Also androgen effects were inhibited due to the reduced level of free (unbound) testosterone and 5α-dihydrotestone.     

Pituitary-testicular axis abnormalities in immature male hypothyroid rats

The pituitary-testicular disturbances which follow the onset of hypothyroidism were studied in immature male Wistar rats rendered hypothyroid by treatment with methimazole (MMI) given in drinking water, starting at 40 days of age. Half of the animals continued on MMI (MMI group) up to 140 days of age; the remaining rats were withdrawn MMI at 100 days and injected thereafter s.c. with 3 micrograms of T3 daily, during the last 40 days (MMI + T3 group). Ten rats were used as controls (C group). Hypothyroidism induced in immature animals significantly decreased serum T4, T3, LH, PRL, and testosterone levels, and also impaired the normal growth of body and sex accessory glands. T3 replacement therapy helped to normalize serum hormonal levels, but the body and sex accessory gland weights were not fully corrected. Hypothyroidism also reduced the [125I]LH/hCG binding sites of testicular homogenates. T3 replacement was not able to improve the binding; nonetheless, the hormone-receptor affinity constant remained unaltered among the groups. Leydig cell responsiveness to hCG stimulation in vitro (0-82 nM) showed impaired testosterone production in the MMI group (25% of that found in the C group) and also in the MMI + T3 group (80% of that found in the C group). These data demonstrate that induction of hypothyroidism in the immature male rat leads to alterations in serum LH, PRL and testosterone levels, and suggest that thyroid hormones have a modulating action on the testis as far as LH-mediated testosterone secretion is concerned.     

Effects of castration and sex steroids on sexually dimorphic development of the mouse submandibular gland

The aims of this study were to characterize sexual dimorphism in the submandibular glands of young adult mice and to determine how sex differences arise during postnatal development. In the mouse submandibular glands, prominent sexual dimorphism was observed at 30 days of age, when the male gland was superior in both the relative occupied area (ROA) and the mitotic rate of the granular convoluted tubules (GCT) to those of the female. By neonatal castration, this sexual dimorphism was abolished, and the intraglandular structures of castrated males were similar to those of normal females. In castrated mice of both sexes, daily treatment with testosterone and 5 alpha-dihydrotestosterone for 10 days from 20 days induced only the ROA of the GCT to increase to the normal male levels but not those of the other three regions of the glands, the acini, intercalated ducts and excretory striated ducts. Testosterone responsiveness of the glands, considering both the glandular weight gain and the mitotic rate of the GCT, was significantly higher in castrated males than in castrated females. On the other hand, 17 beta-estradiol had no effect on the glands of castrated mice. Therefore, the present study suggests that the testicular hormones are responsible for the masculine development of GCT of the glands, but not the ovarian hormones, and that there is a sex difference in the responsiveness of the glands to testosterone, which is more effective in males than in females.     

Influence of 50 Hz magnetic field on sex hormones and other fertility parameters of adult male rats

The effects of an extremely low frequency (ELF) magnetic field on the sex hormones and other fertility parameters of adult male Sprague-Dawley rats were investigated. Adult male rats were exposed to a 50 Hz sinusoidal magnetic field at approximately 25 microT (rms) for 18 consecutive weeks. There were no significant effects on the absolute body weight and the weight of the testes of the exposed rats. However, the weights of seminal vesicles and preputial glands were significantly reduced in the exposed male rats. Similarly, a significant reduction in sperm count was observed in the exposed group. Furthermore, there were no significant effects on the serum levels of male follicle stimulating hormone (FSH) during the 18 weeks of exposure period. On the other hand, there was a significant increase in the serum levels of male luteinizing hormone (LH) after 18 weeks of exposure (P < .005), while testosterone levels were significantly decreased only after 6 and 12 weeks of the exposure period. These results suggest that long term exposure to ELF could have adverse effects on mammalian fertility and reproduction.     

Testosterone and estradiol up-regulate androgen and estrogen receptors in immature and adult rat thyroid glands in vivo

Thyroid gland is one of the non-classical target organs for sex steroids. Presence of androgen and estrogen receptors in the neoplastic and non-neoplastic thyroid glands of mammalian species is well documented. The aim of the present study is to elucidate the changes in serum and thyroidal sex steroids, and their receptors in the thyroid gland of rats from immature to adult age under gonadectomized (GDX) and sex steroids replaced conditions. Normal Wistar male and female rats from immature to adult age (day 21, 30, 45, 60 and 160 post-partum (pp)) were used in the present study. One group (I) of rats was GDX at an early age (day 10 pp) and the other group (II) at the adult age (day 120 pp). Group I rats were sacrificed at different experimental periods such as 21, 30, 45 and 60 days pp, and group II rats were sacrificed at day 160 pp. Another group of GDX rats from group I and II were replaced with physiological doses of testosterone or estradiol. Serum and thyroidal concentrations of sex steroids were estimated by RIA method and the concentrations of receptors by radioreceptor assay. Gonadectomy significantly decreased serum and thyroidal testosterone and estradiol and concentrations of androgen receptor (AR) and estrogen receptor (ER) in the thyroid. Replacement of sex steroids to GDX rats restored the normal level of sex steroids, AR and ER. Therefore, it is suggested from the present study that (i). sex steroids up-regulate their own receptors in the thyroid, (ii). sex steroids may influence thyroid growth and the proliferation of thyrocytes by modulating their receptor concentrations in the thyroid.