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。     

120例肝源性糖尿病患者临床特点分析

目的:探讨肝源性糖尿病的临床特点及其治疗,以提高对该病的诊疗水平.方法:120例肝源性糖尿病(HD)患者,其中46例行OGTT试验,检测了血糖、胰岛素、C肽、胰岛素敏感指数(ISI),HOMA-IR及空腹血糖、空腹胰岛素(FPG/FINS)评估胰岛素抵抗,并与50例2型糖尿病(T2DM)患者进行对比分析.结果:21例(17.5％)HD患者有三多一少糖尿病典型症状.OGTT结果显示HD组空腹血糖低于T2DM组(P＜0.05);胰岛素+C肽释放试验显示T2DM组和HD组胰岛素分泌呈高峰延迟型,HD患者各时段胰岛素及C肽水平高于T2DM患者(P＜0.05,P＜0.01).HD组的FPG/FINS及HOMA-IR低于HD组,ISI高于HD组,差异均有统计学意义(P＜0.05).经治疗后血糖大部分控制在正常或接近正常水平,9例病例均死于肝病并发症.结论:胰岛素抵抗可能是肝源性糖尿病重要的发病机制.肝源性糖尿病以餐后高血糖为特征,临床症状不典型,短期不良预后主要与原发慢性肝病有关.     

2 型糖尿病患者血浆成纤维细胞生长因子-21 水平的变化及意义

目的:探讨2型糖尿病(type 2 diabetes mellitus,T2DM)患者血浆成纤维细胞生长因子-21(fibroblast growth factor 21,FGF-21)水平变化以及观察短期胰岛素强化治疗对FGF-21水平的影响。方法:选择我院2013年1月至2015年1月收治的T2DM患者64例,其中初诊T2DM患者32例(T2DM组),T2DM合并大血管病变患者32例(合并大血管病变组),并选择同期体检健康者30例(对照组)。采用酶联免疫法测定三组血浆FGF-21水平以及胰岛素强化治疗前后的变化,分析血浆FGF-21水平与体质量指数(BMI)、腰臀比(WHR)、血脂、血糖、空腹血浆胰岛素(FINS)和糖化血红蛋白(Hb A1C)等水平的关系。结果:T2DM组及T2DM合并大血管病变组患者空腹血浆FGF-21水平明显高于对照组(P0.05),T2DM合并大血管病变组患者空腹血浆FGF-21水平明显高于T2DM组和对照组(P0.05)。空腹血浆FGF-21水平与T2DM患者FPG、Hb A1C水平呈明显正相关,WHR、舒张压、Hb A1C是影响血浆FGF-21水平的独立相关因素。经胰岛素强化治疗后,血浆FGF-21水平较治疗前明显下降(P0.05)。结论:T2DM患者血浆FGF-21水平明显升高,可能参与了T2DM及其大血管病变的发生和发展,胰岛素强化治疗可明显降低T2DM患者血浆FGF-21水平,血浆FGF-21可能作为T2DM病情和疗效评估的参考指标。     

链脲佐菌素诱导长爪沙鼠Ⅰ型糖尿病模型的实验研究

目的探讨链脲佐菌素(STZ)诱导长爪沙鼠Ⅰ型糖尿病模型的可能性,并观察模型动物早期肾脏损害情况。方法雄性长爪沙鼠96只,随机分为正常对照组(NC组)、模型组1(DM1组)、模型组2(DM2组),DM1及DM2组沙鼠分别一次性腹腔注射100 mg/kg、200 mg/kg STZ,NC组注射等量柠檬酸盐缓冲溶液。注射STZ后1、2、4、6周末,分别监测沙鼠一般情况,血糖、胰岛素等血清学指标和尿液指标,并处死沙鼠进行胰腺和肾脏组织的病理学检查。结果注射STZ 24 h后,DM2组及DM1组部分沙鼠逐渐出现典型的"三多一少"症状,随着病程的发展,DM2组沙鼠持续高血糖,DM1组沙鼠血糖值与NC组差异有显著性(P0.05),但有下降趋势;DM2组沙鼠胰岛素显著性降低(P0.05),其他血清学指标及尿液指标均显著性升高(P0.05),DM1组沙鼠各指标差异无显著性。DM2组沙鼠及DM1组少数沙鼠胰腺组织中可见胰岛β细胞减少、空泡样变性等变化,DM2组沙鼠肾脏组织中出现肾小球基质增多,毛细血管襻扩张等病变,DM1组沙鼠肾脏组织未见明显变化。结论 STZ 200 mg/kg可成功诱导长爪沙鼠Ⅰ型糖尿病模型,在病程早期沙鼠肾脏结构和功能已经发生改变。     

2型糖尿病大鼠心肌IR、IRS-1的表达与罗格列酮及APP5肽类似物P165的干预效应

目的研究2型糖尿病大鼠心肌胰岛素信号转导通路蛋白胰岛素受体（IR）、胰岛素受体底物-1（IRS-1）的表达与正常SD大鼠的区别,并探讨进行罗格列酮及APP5肽类似物P165干预后对上述蛋白表达的影响。方法60只SD大鼠随机分为正常对照组（C组）、正常对照＋罗格列酮组（C＋RSG组）、2型糖尿病组（T2DM组）、2型糖尿病＋罗格列酮组（T2DM＋RSG组）、糖尿病给予P165小剂量组（T2DM＋P165小剂量组）、糖尿病给予P165大剂量组（T2DM＋P165大剂量组）,其中糖尿病动物采用高脂饮食后给予小剂量STZ腹腔注射的方法造模。后将各组SD大鼠处死,采用免疫组织化学染色和Western blot的方法检测心肌组织IR、IRS-1的表达。结果（1）2型糖尿病组（T2DM组）心肌组织IR、IRS-1的表达水平显著低于对照组（C组）;（2）2型糖尿病＋罗格列酮组（T2DM＋RSG组）心肌组织IR、IRS-1的表达水平显著高于T2DM组;（3）免疫组化染色发现2型糖尿病＋P165小/大剂量组（T2DM＋P165小/大剂量组）心肌组织IR、IRS-1免疫反应阳性颗粒沉着的累积光密度值显著高于T2DM组;Western blot结果显示T2DM＋P165小/大剂量组心肌组织IRS-1的表达水平显著高于T2DM组;而IR的表达水平与T2DM组相比无差别。结论（1）2型糖尿病大鼠心肌存在胰岛素抵抗或信号转导障碍;（2）罗格列酮干预后可以改善2型糖尿病心肌的胰岛素信号转导异常;（3）P165对2型糖尿病大鼠心肌胰岛素信号转导具有调节作用,其作用靶点可能为胰岛素受体底物。     

不同剂量链尿佐菌素诱导2型糖尿病大鼠模型的研究

目的:探讨不同剂量链脲佐菌素(Streptozotocin,STZ)联合高糖高脂饮食对2型糖尿病大鼠模型建立的影响。方法:90只8周龄SD雄性大鼠随机平均分为六组:普通饲料喂养+缓冲液组、高糖高脂饲料喂养+缓冲液(H.E组)、高糖高脂饲料喂养+35mg/kg链尿佐菌素组(H.E+35 mg/kg STZ组)、高糖高脂饲料喂养+45 mg/kg链尿佐菌素组(H.E+45 mg/kg STZ组)、高糖高脂饲料喂养+55 mg/kg链尿佐菌素组(H.E+55 mg/kg STZ组)及高糖高脂饲料喂养+65 mg/kg链尿佐菌素组(H.E+65 mg/kg STZ组),高糖高脂饲料喂养4周后诱导胰岛素抵抗,继之腹腔注射STZ,建立2型糖尿病大鼠模型。检测体重、胰岛素、空腹血糖、血脂、胰岛素敏感指数(ISI)。结果:与常规饮食组相比,高糖高脂饮食各组大鼠出现空腹血浆胰岛素(FINS)、空腹血糖(FBG)、血清甘油三脂(TG)、总胆固醇(TC)、游离脂肪酸(FFA)显著升高(P0.01),ISI显著下降(P0.01)。不同剂量STZ注射,H.E+45 mg/kg STZ组成模率最高且无自愈现象。结论:通过STZ腹腔注射联合高糖高脂饮食可成功复制出实验性2型糖尿病动物模型,45 mg/kg为STZ理想注射剂量。     

改善Ⅱ型糖尿病大鼠糖代谢运动模型的建立

目的建立运动改善Ⅱ型糖尿病大鼠糖代谢模型,为Ⅱ型糖尿病运动处方的建立提供理论参考。方法 SPF级雄性8周龄Wistar大鼠45只,随机抽取32只在高糖高脂饲料喂养7周的基础上腹腔注射小剂量链脲佐菌素(STZ)缓冲液,建立Ⅱ型糖尿病大鼠模型。将正常大鼠和造模成功的大鼠分为4组:空白对照组(C组)、单纯运动组(CE组)、糖尿病对照组(DM组)、糖尿病运动组(DME组)。运动组采用改进的Ploug训练方案,60min/d,每周训练6 d,共训练8周。分别在高脂饲料喂养7周后尾静脉取血测定空腹血糖和血清胰岛素,造模后基线时间和运动8周末尾静脉取血测定空腹血糖(FBG),运动8周末眶后取血测定血清胰岛素(FINS),并计算胰岛素抵抗指数(HOMA-IR)。结果 (1)7周高糖高脂喂养后,与正常组相比,高脂组FBG、FINS和HOMA-IR含量显著升高。(2)8周运动干预后,DM组和DME组FINS水平显著低于C组和CE组,FBG和HOMA-IR显著高于C组和CE组;DME组FINS水平显著高于DM组,FBG和HOMA-IR显著低于DM组。DM组和DME组体重显著低于C组和CE组;DME组与DM组、CE组与C组组间体重差异无显著性。结论 (1)7周高糖高脂喂养联合一次性腹腔注射STZ(30 mg/kg)成功建立Ⅱ型糖尿病大鼠模型;(2)60 min/d共8周的游泳运动模式能够改善Ⅱ型糖尿病大鼠糖代谢,是研究运动锻炼预防和改善糖尿病机理的理想动物模型。     

糖尿病大鼠性腺及外周血中性激素的改变

目的:研究糖尿病大鼠性腺及外周血中性激素的变化。方法:用放射免疫法检测糖尿病(DM)大鼠,正常(NDM)大鼠和STZ大鼠血清性激素含量,同时称取性腺重量,镜检睾丸、前列腺及附睾的组织形态学改变。结果:DM组睾酮水平显著低于NDM组、STZ组(P<0.01);NDM组与STZ组之间,睾酮水平无显著性差异;DM组促黄体生成素(LH)水平显著高于NDM组、STZ组(P<0.01);NDM组与STZ组之间。LH水平无显著性差异;促卵泡刺激素(FSH)水平在各组之间无显著性差异;HE结果显示,DM组性腺显微结构较NDM组及STZ组明显改变。结论:提示DM严重影响大鼠性腺功能及睾酮的合成分泌,并显著降低大鼠血清睾酮含量。     

高脂饲喂联合链脲佐菌素诱导的Beagle犬糖尿病模型

目的应用高脂饲喂联合链脲佐菌素(STZ)构建Beagle犬T2DM模型,并观察其相关特征。方法将普通级雄性Beagle犬30只随机分为3组:对照组,高脂组,糖尿病模型组,每组10只。糖尿病模型组饲喂高脂饲料同时在饲喂2个月时注射STZ;高脂组饲喂高脂饲料;对照组饲喂普通饲料,连续饲喂5个月。定期测定动物Lee指数、空腹血糖、胰岛素、尿糖,并在3月时进行OGTT试验,试验结束后进行血脂等血液生化检测和肝、胰腺组织病理检查。结果高脂组和糖尿病模型组高脂饲养2个月后Lee指数显著增加(P0.01),并出现高胰岛素血症和胰岛素抵抗伴血脂异常;糖尿病模型组STZ注射后空腹血糖显著升高(P0.01),且持续3个月维持在高血糖水平;而高脂组的空腹血糖无明显变化(P0.05),糖尿病模型组OGTT试验3 h血糖值11.1mmol/L,且3 h未恢复,胰腺组织病理学检查出现一定程度的损伤和病变。结论高脂饲料饲喂诱导Beagle犬胰岛素抵抗和高血脂症,但未能形成高血糖状态,而高脂饲料饲喂联合注射STZ后Beagle犬在出现高血脂症的同时发生胰岛素抵抗,与人类T2DM的胰岛素抵抗伴高血糖、高胰岛素血症和高血脂等典型症状相似。     

链脲佐菌素诱导C57BL/6J小鼠2型糖尿病模型研究

目的建立与2型糖尿病(非胰岛素依赖型糠尿病、NIDDM)病人临床特征和发病过程相似的NIDDM动物模型.方法用高脂肪饲料喂养C57BL/6J雄性断乳小鼠3周,腹腔注射链脲佐菌素(STZ),继续喂养4周,测定给药前和给药后1、3、4周非空腹血糖、实验结束时非空腹胰岛素水平,观察胰腺形态学变化.结果喂养3周后(给药前)高脂饲料-STZ组及高脂饲料-柠檬酸组血糖浓度(7.0±0.39)mmol/L、( 6.8±0.45)mmol/L高于普通饲料-STZ组及普通饲料-柠檬酸组(5.3±0.40)mmol/L、(5. 4±0.39)mmol/L,P＜0.05;实验结束时,高脂饲料-STZ组血糖浓度(13 .1±2.01)mmo/L高于高脂饲料-柠檬酸(6.9±0.46)mmol/L、普通饲料-柠檬酸组(6.0± 0.46)mmol/L和普通饲料-STZ组(7.1±0.62)mmol/L(P＜0.05),各组间血浆胰岛素浓度、体重及饮水量差异无显著性,P＞0.05;实验过程中高脂饲料STZ组和柠檬酸组小鼠每天进食热量(64.49±9.2)kJ/只,(70.7±9.6)kJ/只, 显著高于普通饲料STZ组和柠檬酸组(52.7±7.9)kJ/只,(57.3±11.7)kJ/只;各组小鼠胰腺和胰岛细胞形态正常.结论高脂肪饲料和STZ是用C57BL/6J断乳幼鼠建立NIDDM模型所必须的,100mg/kg体重STZ对普通饲料小鼠血糖无影响;用高脂饲料和STZ 处理的小鼠血糖升高、胰岛素浓度正常,与NIDM病人临床特征和发病过程相似;C57BL/6J小鼠易得,建模方法简便,费用低,是在NIDDM实验研究中能广泛使用的较理想的非遗传性NID DM动物模型.     

Antioxidant icariside II combined with insulin restores erectile function in streptozotocin‐induced type 1 diabetic rats

Erectile dysfunction (ED) worsens in patients with diabetes mellitus (DM) despite good control of blood glucose level with insulin. Recent studies imply that diabetic vascular stresses (e.g. oxidative stress) persist in spite of glucose normalization, which is defined as metabolic memory. Studies suggest that the interaction between advanced glycation end products (AGEs) and their receptor (RAGE) mediates the development of metabolic memory. To investigate the effects of the antioxidant icariside II plus insulin on erectile function in streptozotocin (STZ)‐ induced type 1 diabetic rats. Fifty 8‐week‐old Sprague‐Dawley rats were randomly distributed into five groups: normal control, diabetic, insulin‐treated diabetic, icariside II‐treated diabetic, and insulin plus icariside II‐treated diabetic. Diabetes was induced by a single intraperitoneal injection of STZ. Eight weeks after induction of diabetes, icariside II was administered by gastric lavage once a day (5 mg/kg) for 6 weeks; and 2–6 units of intermediate‐acting insulin were given to maintain normal glycemia for 6 weeks. The main outcome measures were the ratio of intracavernous pressure (ICP) to mean arterial pressure (MAP); histology of penile endothelial cells and smooth muscle cells; neural nitric oxide synthase, AGEs and RAGE expression; malondialdehyde concentration; superoxide dismutase activity; and apoptosis index. Diabetic rats demonstrated a significantly lower ICP/MAP ratio, reduced penile endothelial cells, reduced smooth muscle cells, increased AGEs and RAGE, and increased apoptosis. Insulin and icariside II monotherapy partially restored erectile function and histological changes. However, the combination therapy group showed significantly better erectile parameters, cytological components and biochemistry, similar to those in the normal control group. These results suggest that, although insulin can effectively control glycemic levels, it does not completely alter the pathological changes in erectile tissues. Better efficacy could be expected with tight glycemic control plus the antioxidant icariside II. The proposed combination therapy might have the potential to eliminate metabolic memory by down‐regulating the AGEs‐RAGE‐oxidative stress axis.     

Studies on the mechanism of testicular dysfunction in the early stage of a streptozotocin induced diabetic rat model

Streptozotocin (STZ) induced diabetic model has been widely used to study the effects of diabetes mellitus (DM) on male infertility, but it remains unclear whether the responses in this model are due to hyperglycemia or STZ per se. This study was designed to investigate the mechanism of STZ on testicular dysfunction. In the present study, sperm characteristics, serum testosterone, steroidogenic enzymes (StAR and 3β-HSD), and the vimentin apical extension of sertoli cells decreased significantly in the STZ group compared with those in the normal controls (p < 0.05), while Johnsen’s score, testicular lipid peroxidation, spermatogenic cell apoptosis, and the expressions of NF-κB and Wnt4 significantly increased (p < 0.05). Insulin replacement mainly restored the decreased serum testosterone and steroidogenic enzymes, but not other parameters. The results indicated that spermatogenic dysfunction in the early stage of STZ-induced diabetic rats was due to direct STZ cytotoxicity to sertoli cells, which could be regulated by Wnt4 and NF-κB, while steroidogenic dysfunction might be a direct or indirect consequence of insulin deficiency. The results suggested that STZ-induced diabetic model, at least in the early stage, is not suitable to study the diabetes-related spermatogenic dysfunction.     

Testosterone selectively increases serum follicle-stimulating hormonal (FSH) but not luteinizing hormone (LH) in gonadotropin-releasing hormone antagonist-treated male rats: evidence for differential regulation of LH and FSH secretion

Both testosterone (T) and gonadotropin-releasing hormone (GnRH)-antagonist (GnRH-A) when given alone lower serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in intact and castrated rats. However, when graded doses of testosterone enanthate (T.E.) were given to GnRH-A-treated intact male rats, a paradoxical dose-dependent increase in serum FSH occurred; whereas serum LH remained suppressed. This surprising finding led us to ask whether the paradoxical increase in serum FSH in GnRH-A-suppressed animals was a direct stimulatory effect of T on the hypothalamic-pituitary axis or the result of a T effect on a testicular regulator of FSH. To test these hypotheses, we treated adult male castrated rats with GnRH-A and graded doses of T.E. In both intact and castrated rats, serum LH remained undetectable in GnRH-A-treated rats with or without T.E. However, addition of T.E. to GnRH-A led to a dose-dependent increase in serum FSH in castrated animals as well, thus pointing against mediation by a selective testicular regulator of FSH. These data provide evidence that pituitary LH and FSH responses may be differentially regulated under certain conditions. When the action of GnRH is blocked (such as in GnRH-A-treated animals), T directly and selectively increases pituitary FSH secretion.     

Some effects of experimentally-induced diabetes on pituitary-testicular relationships in rats.

The effect of experimentally-induced diabetes mellitus on reproductive organ weights, serum and pituitary gonadotropin levels and serum testosterone levels was studied in 3-month old rats. In experiment 1, intact rats were treated with alloxan monohydrate or streptozotocin. In experiments 2 and 3, intact and castrated rats were rendered diabetic with alloxan (experiment 2) or streptozotocin (experiment 3). The duration of each experiment was 3 weeks. In each experiment diabetes resulted in body weight losses or reduced body weight gain, elevated serum glucose concentrations and reduced assessory sex gland weights (intact rats). Serum levels of testosterone were depressed (P less than 0.05 or P less than 0.01) in diabetic rats. Serum levels of LH were significantly (P less than 0.05) lower in intact diabetics than in controls when pooled data from the three experiments were compared. Serum levels of FSH were not affected by diabetes. Pituitary concentrations of FSH were elevated (P less than 0.05) in diabetics in two of the three experiments, while LH concentrations were elevated (P less than 0.05 or P less than 0.01) in diabetics in all experiments. The hypersecretion of gonadotropins in castrated rats was not affected by diabetes.     

Knockdown of miR-423-5p simultaneously upgrades the eNOS and VEGFa pathways in ADSCs and improves erectile function in diabetic rats

This study aimed to explore the possibility of miR-423-5p modified adipose-derived stem cell (ADSCs) therapy on streptozotocin (STZ)-induced diabetes mellitus erectile dysfunction (DMED) rats. MiR-423-5p was knocked down in ADSCs. ADSCs, NC-miR-ADSCs and miR-ADSCs were co-cultured with human umbilical vein endothelial cells (HUVECs). Normal and high glucose media were supplemented. The supernatant and HUVECs were collected for assessment of eNOS and VEGFa expression, cell proliferation, and apoptosis. HUVECs co-cultured with ADSCs or miR-ADSCs exhibited higher eNOS and VEGFa protein expression levels compared to DM groups. MiR-ADSCs enhanced HUVEC proliferation compared to the ADSCs and NC-miR-ADSCs. Lower apoptotic rates were observed when HUVECs were co-cultured with miR-ADSCs, compared to ADSCs and NC-miR-ADSCs. Fifteen male Sprague-Dawley (SD) rats aged 12 weeks were induced to develop diabetes mellitus by intraperitoneal injection with STZ, and five healthy SD rats were used as normal controls. Eight weeks after developing diabetes, the rats received ADSCs and miR-ADSCs via injection into the corpora cavernosa, whereas normal controls and DM controls were injected with saline. Erectile function and histological assessment of penile tissues were performed 8 weeks after injection. The ICP/MAP indicated that erectile function was impaired in the DM rats compared with the normal group. Injection of ADSCs and miR-ADSCs improved erectile function significantly and was associated with the overexpression of eNOS and VEGFa. MiR-423-5p knockdown in ADSCs ameliorated high glucose-mediated damage to HUVECs and improved erectile function in DM rats by inducing eNOS and VEGFa overexpression, indicating that miR-423-5p may be a potential target in the treatment of DMED.     

急、慢性运动对2型糖尿病大鼠脂肪PI3K/AKT/GLUT4通路的影响

目的:探讨急性和慢性运动对2型糖尿病(T2DM)大鼠脂肪组织明磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)/葡萄糖运载体4(GLUT4)信号通路的影响。方法:15月龄SD雄性大鼠52只随机分为正常对照组(n=13)和高脂组(n=39),分别喂养普通和高脂饲料。8周后,高脂组体重＞正常对照组20％,注射小剂量STZ后,血糖＞16.7 mmol/l,造模成功。将糖尿病模型组随机分为糖尿病对照组(DC,n=13),糖尿病慢性运动组(DCE,n=13),糖尿病急性运动组(DAE,n=13)。DCE组进行8周的游泳运动,DAE组进行一次性游泳运动。测定血脂,血糖和血清胰岛素,Western blot法测定脂肪PI3K、AKT和GLUT4蛋白含量。结果:糖尿病组体重、血脂、血糖、胰岛素显著高于正常对照组(P均＜0.01);高密度脂蛋白胆固醇(HDL-C)水平降低(P＜0.05),脂肪组织中PI3K、AKT和GLUT4蛋白表达下降(P均＜0.01)。糖尿病慢性运动组体重、血脂、血糖、胰岛素均出现显著性下降(P均＜0.01);HDL-C升高(P＜0.05),脂肪PI3K、AKT和GLUT4蛋白表达上升(P＜0.01)。糖尿病急性运动组血脂、血糖、胰岛素下降(P均＜0.05);HDL-C升高(P＜0.05),脂肪PI3K、AKT和GLUT4含量显著上升(P均＜0.05)。结论:①高脂饮食结合小剂量STZ诱导的T2DM大鼠脂肪组织PI3K/AKT通路受损,降低了胰岛素的敏感性。②急性、慢性有氧运动,均可以通过PI3K/AKT通路,改善糖脂代谢紊乱,慢性运动略优于急性运动。     

Effects of unilateral castration on serum luteinizing hormone, follicle stimulating hormone, and testosterone concentrations in one-, two-, and three-year-old stallions

The endocrine control of compensatory hypertrophy was investigated in 12 Morgan stallions, four each at one, two and three years of age. Half were assigned to be unilaterally castrated (UC) in January and half to remain intact (IN). Nine blood samples were taken from each stallion at half-hour intervals 30, 90, and 150 d after unilateral castration for radioimmunoassay of serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), and testosterone. Mean serum LH concentration was greater (P<0.06) in UC than IN stallions; however, the difference was greatest at 30 d and least at 150 d. Serum LH was greater (P<0.01) in two- and three-year-olds than in one-year-olds. The mean log(10) for serum FSH concentration was greater (P<0.06) in UC than IN stallions. Mean serum testosterone concentrations were similar in UC and IN stallions for all sample days, suggesting that the single testes of the UC stallions produced as much testosterone as the two testes of the IN stallions. Two- and three-year-old stallions had greater (P<0.01) serum testosterone than one-year-old stallions. Unilateral castration of stallions was associated with a significant increase in serum LH and FSH concentrations and, perhaps, higher intratesticular testosterone, which may explain, in part, the compensatory hypertrophy noted in the remaining testis.     

Gonadal function in male mountain bikers

Some studies reported testicular disorders associated with biking in mountain cyclists, which include injuries, erectile dysfunction, and higher scrotal temperatures. But none of these studies evaluated gonadal function. Therefore, the aim of this study was to evaluate gonadal function in male mountain bikers. Twenty-two male professional mountain bikers and 30 healthy noncyclist controls were included in the study. The mean age and body mass index were similar in both groups. Fasting blood samples for the measurement of the levels of total testosterone (TT), sex-hormone binding globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were obtained from all study participants before any physical activity. In addition, because insulin sensitivity and leptin modulate gonadal function, the concentrations of insulin, glucose, and leptin were also measured in the same samples. Calculated free testosterone (cFT) and bioavailable testosterone (bioT) were calculated from SHBG and TT. Basal hormonal levels including insulin, leptin, LH, FSH, SHBG, TT, glucose, and homeostasis model assessment scores were similar between the groups. However, bioT and cFT levels were significantly lower (p ≤ 0.05) in the mountain bikers than those in the controls. Despite the lower mean testosterone levels in the study group, the levels of LH and FSH were similar to controls. Insulin and leptin do not contribute to lower testosterone levels. In conclusion, male mountain bikers have lower testosterone concentrations compared to controls. This alteration cannot solely be explained by testicular dysfunction. The etiology of lower testosterone levels in cyclists appears to be complex and requires further research. The influence of such a decline on the athlete's performance, quality of life, and muscle strength is not known as yet.