颗粒蛋白前体在高脂饮食诱导的肥胖PCOS大鼠卵巢中的表达

目的研究颗粒蛋白前体(PGRN)在肥胖PCOS大鼠卵巢中的表达情况,初步探讨PGRN在PCOS发病中的作用。方法选择SPF级23日龄SD雌性大鼠38只,使用随机数字表随机分为3组:正常对照组(n=8)、PCOS组(DHEA组,n=15)及肥胖PCOS组(DHEA+HFD组,n=15)。采用脱氢表雄酮联合高脂饲料(DHEA+HFD)诱导肥胖PCOS大鼠。HE染色光镜下观察PCOS大鼠卵巢的病理结构改变。酶联免疫吸附法测定血清睾酮(T)、雌二醇(E2)及空腹血糖(FBG)、空腹胰岛素(FINS)含量等,比较各组间的水平差异。采用免疫组织化学法检测各组卵巢PGRN的表达水平及分布情况。结果造模结束时,DHEA+HFD组体重显著高于对照组(P<0.01)及DHEA组(P<0.05)。DHEA组及DHEA+HFD组的FINS、稳态模型评估的胰岛素抵抗指数(HOMA-IR)均显著高于对照组(P<0.05)。DHEA组及DHEA+HFD组的睾酮(T)、FSH水平均显著升高(P<0.01)。DHEA组及DHEA+HFD组卵巢组织光镜下均表现出典型的多囊样改变。免疫组化结果显示各组大鼠卵巢中均可见PGRN蛋白表达,主要分布于卵泡的颗粒细胞层及黄体;DHEA组PGRN表达水平显著高于对照组(P<0.01),DHEA+HFD组PGRN表达水平显著高于DHEA组及对照组(P<0.01)。结论 PGRN在卵巢颗粒细胞层有表达。其在PCOS大鼠和肥胖PCOS大鼠卵巢组织中的差异性表达,提示PGRN可能通过作用于局部卵泡微环境,参与PCOS肥胖及慢性代谢性炎症的发生。     

高脂高糖饮食暴露诱导大鼠多囊卵巢综合征研究

目的通过高脂高糖饮食诱导雌性大鼠多囊卵巢综合征(PCOS),探讨其生殖和代谢特征。方法将23天断奶雌性大鼠随机分成两组:对照组接受正常饮食(对照组,n=18),实验组接受高脂高糖饮食(HFHS组,n=18),连续喂养14周。观察两组体重、动情周期和卵巢组织学变化,检测两组空腹血糖、空腹胰岛素、计算胰岛素抵抗指数(HOMA-IR)、血脂水平、性激素水平。结果 HFHS组大鼠体重至第3周起显著高于对照组(P0.001),但两组卵巢重量无显著差异[(0.041±0.006)g vs.(0.045±0.005)g,P0.05]。HFHS组动情周期失去规律变化,发情期持续时间占整个发情周期时间的比例显著长大对照组[(0.46±0.06)vs.(0.27±0.03),P0.001]。HFHS组卵巢组织学检查发现多个囊状扩张卵泡、黄体数量下降。HFHS组空腹胰岛素、HOMA-IR、总胆固醇水平显著高于对照组(P0.001);发情间期HFHS组LH和E2水平显著低于对照组(P0.05),睾酮(T)水平显著高于对照组(P0.001);发情前期HFHS组LH和P水平显著低于对照组(P0.05),T和E2水平显著高于对照组(P0.001)。结论高脂高糖饮食诱导雌性大鼠PCOS,并产生代谢紊乱和卵巢改变,与PCOS患者临床观察到的相似。     

ATP合成酶β亚单位在PCOS伴2型糖尿病大鼠胰岛中的表达

目的研究ATP合成酶β亚单位在多囊卵巢综合征(PCOS)伴2型糖尿病的大鼠胰岛中的表达情况,初步探讨ATP合成酶β亚单位在PCOS发展为2型糖尿病中的作用。方法 30只雌性SD大鼠平均分为3组:PCOS组、PCOS伴2-DM组和对照组。采用硫酸普拉睾酮钠诱导PCOS模型(PCOS组,10只),硫酸普拉睾酮钠联合高脂高糖+链脲左菌素(STZ)诱导2型糖尿病大鼠模型(PCOS伴2-DM组,10只)。HE染色光镜下观察PCOS大鼠卵巢的病理结构改变,用酶联免疫吸附法测定血清睾酮(T)、雌二醇(E2)及空腹血糖(FBG)、空腹胰岛素(FINS)含量。采用免疫组织化学法检测PCOS组、PCOS伴2型糖尿病组及空白对照组胰腺胰岛中ATP合酶β亚单位的表达。结果与对照组相比,PCOS伴2-DM组及PCOS组卵巢均呈多囊样改变;与对照组相比,PCOS伴2-DM组和PCOS组大鼠FINS虽显著降低(P0.05),但HOMA-IR指数均显著增高(P0.05),PCOS伴2-DM组大鼠空腹血糖均≥16.7mmol/L;PCOS组及PCOS伴2-DM组大鼠血清T与E2水平显著高于对照组(P0.05),而PCOS组及PCOS伴2-DM组之间无显著差异(P0.05);PCOS伴2-DM组的胰岛面积显著小于对照组及PCOS组(P0.05);PCOS伴2-DM组ATP合酶β亚单位的表达强度显著低于对照组及PCOS组(P0.05),PCOS组与对照组相比胰岛中ATP合酶β亚单位的表达亦显著降低(P0.05)。结论硫酸普拉睾酮钠联合高脂高糖饮食+小剂量STZ能有效诱导PCOS伴2型糖尿病大鼠模型;PCOS及PCOS伴2型糖尿病患者胰岛中ATP合成酶β亚单位表达异常,可能是导致2型糖尿病发生的原因之一。     

一种新的胰岛素抵抗的多囊卵巢综合征大鼠模型的建立

目的皮下注射脱氢表雄酮（DHEA）联合高脂高卡饮食喂养,建立一种新的胰岛素抵抗（IR）的多囊卵巢综合征（PCOS）大鼠模型。方法建立60只IR的PCOS雌鼠为造模组,13只同龄雌鼠为对照组。HE染色观察卵巢形态学变化,葡萄糖氧化酶法测定空腹血糖（FBG）,ELISA检测胰岛素样生长因子（IGF）-I、胰岛素样生长因子结合蛋白（IGFBPs）,放射免疫法测定血清空腹胰岛素（Fins）、睾酮（T）、雌二醇（E2）、卵泡刺激素（FSH）、黄体生成素（LH）,计算胰岛素敏感指数（ISI）和LH／FSH。结果与对照组比较,造模组大鼠卵巢呈多囊样改变,平均排卵数及排卵率、IGF-1、IGFBP-3、ISI、FSH明显降低（P〈0．05或P〈0．01）,FBG、Fins和IGFBP-1、T、E2、LH浓度以及LH／FSH显著升高（P〈0．05或P〈0．01）。结论皮下注射DHEA联合高脂高卡饮食,可成功诱导IR的PCOS大鼠模型。     

细胞色素P450芳香化酶在大鼠多囊卵巢中的表达及意义

目的检测细胞色素P450芳香化酶(P450 arom)在大鼠多囊卵巢颗粒细胞中的表达水平,探讨P450 arom与多囊卵巢综合征(PCOS)的关系。方法应用半定量逆转录-聚合酶链反应(RT-PCR)检测PCOS实验组及正常对照组大鼠卵巢组织中P450 arom基因(CYP19)的表达;采用链霉素抗生物素蛋白-过氧化物酶(SP)法对大鼠卵巢组织中P450 arom进行检测。结果实验组和对照组卵巢组织中CYP19基因,相对表达强度分别为(0.138±0.072)和(0.759±0.236),差别有显著性意义(P<0.01);实验组中原始卵泡、初级卵泡和成熟卵泡比较,P450 arom蛋白表达下降(P<0.05)。对照组间初级卵泡、次级卵泡和成熟卵泡比较,arom蛋白表达有显著性差异(P<0.05)。结论P450 arom mRNA在PCOS大鼠卵巢组织中呈低表达;P450 arom蛋白在PCOS大鼠卵巢初级卵泡和成熟卵泡中表达下降;PCOS的发生可能与P450 arom在mRNA和蛋白水平的表达下调有关。     

高雄激素PCOS动物模型中抗苗勒管激素Ⅱ型受体蛋白及其基因甲基化分析

目的通过建立高雄激素诱导的多囊卵巢综合征(PCOS)大鼠模型,探讨抗苗勒管激素Ⅱ型受体(AMHRⅡ)在卵巢、子宫内膜中的表达及其基因启动子区域甲基化与PCOS发病及局部病理变化的关系。方法 45只雌性SD大鼠随机分两组:PCOS组皮下注射脱氢表雄酮(DHEA)建立PCOS模型,对照组同期皮下注射等量生理盐水;测定血清激素水平,结合卵巢组织HE染色切片结构改变评估PCOS模型;免疫组化法检测卵巢、子宫内膜组织AMHRⅡ蛋白的表达与定位;通过甲基化特异性PCR(MSP)定性分析两组大鼠血液、卵巢组织AMHRⅡ基因启动子区域的甲基化状态。结果血清性激素水平及卵巢切片结果均提示成功建立PCOS动物模型;免疫组化检测显示AMHRⅡ蛋白定位表达于细胞膜,在卵巢间质及卵泡颗粒细胞中均存在阳性表达,且在模型组中的表达强于对照组(P0.05);AMHRⅡ在子宫内膜中也存在表达,两组之间表达无统计学差异(P0.05);MSP结果显示两组中血液及卵巢组织所有DNA样本均检出部分甲基化条带,两组之间无统计学差异(P0.05)。结论 AMHRⅡ可能参与了PCOS中AMH调控卵泡发育的过程,但与子宫内膜病变无明显相关性;AMHRⅡ基因在启动子区域存在着部分甲基化,但这种甲基化状态与PCOS发病及局部组织病理变化无明显相关。     

高胰岛素血症与多囊卵巢综合征大鼠排卵障碍的相关性研究

目的探讨高胰岛素血症参与多囊卵巢综合征(PCOS)排卵障碍的可能机制。方法(1)按改良Poretsky法建立PCOS动物模型,采用测定空腹血糖(FBG)、空腹胰岛素(FINS)、睾酮(T)、雌二醇(E2)、黄体生成素(LH)、卵泡刺激素(FSH),并计算胰岛素抵抗指数(HOMA1-IR);HE染色观察卵巢病理变化验证模型。(2)采用免疫组织化学方法检测卵巢组织生长分化因子9(GDF-9)蛋白质的表达。结果(1)与正常对照组比较,高胰岛素血症组FBG、FINS、T、HOMA1-IR显著升高(P<0.01)。(2)高胰岛素血症组各发育阶段卵泡数明显减少,但囊性扩张的卵泡和闭锁卵泡增多,卵泡膜细胞增生,卵泡间的间质明显增厚。(3)高胰岛素血症组卵巢组织GDF-9蛋白质表达显著低于正常对照组(P<0.05)。结论高胰岛素血症可能通过抑制GDF-9在卵巢组织的表达,使卵泡发育停滞、闭锁而导致排卵障碍。     

探究短期去势法对12月龄雌性大鼠骨质的影响

目的初步研究使用切除卵巢法作用于12月龄SD雌性大鼠一个月对其骨质的相关影响。方法将6只12月龄SD雌性大鼠分为2组(实验组3只,假手术组3只),对实验组的大鼠进行切除双侧卵巢操作;对照组的大鼠进行假手术操作,即行腹部切口切除与卵巢重量相同的脂肪组织。术后一个月,分别取出实验组和假手术组大鼠的第3腰椎和左侧股骨,随后进行Micro-CT检测,以了解其骨密度(BMD)、骨小梁相关情况。结果实验组对比假手术组12月龄SD雌性大鼠左侧股骨的皮质骨BMD、松质骨BMD及其总体BMD均有所下降,但无统计学意义(P0.05);实验组对比假手术组12月龄SD雌性大鼠腰3椎体的皮质骨BMD有所下降(P0.05),而腰3椎体的松质骨BMD以及其总体BMD稍有上升(P0.05)。实验组腰3椎体和左侧股骨骨小梁BMD较假手术组下降,但亦无统计学差异(P0.05)。术后一个月无SD雌性大鼠死亡情况。结论对12月龄SD雌性大鼠使用切除卵巢法并饲养观察时间只为一个月难以构造成骨质疏松动物模型。     

PCOS及PCOS伴2型糖尿病大鼠卵巢热休克蛋白70的研究

目的利用量子点(QDs-SA605)荧光及免疫组化法对热休克蛋白(HSP)70进行标记,检测PCOS及PCOS伴2型糖尿病(2-DM)大鼠卵巢中HSP70的表达情况。方法将23日龄雌性SD大鼠分为PCOS组、PCOS伴2-DM组及对照组,PCOS组及PCOS伴2-DM组以硫酸普拉睾酮钠9mg/100g皮下注射20d;PCOS伴2-DM组则在硫酸普拉睾酮钠停药后第2天给予链脲佐菌素(STZ)45mg/kg腹腔注射1次,PCOS组及对照组注射等量柠檬酸盐缓冲液。注射后72h处死大鼠,观察卵巢形态学改变,测定血清性激素、胰岛素及血糖水平,并以QDs-SA605荧光标记和免疫组化染色检测各组大鼠卵巢组织中HSP70的表达。结果血液指标测定结果显示,与对照组相比,PCOS组和PCOS伴2-DM组血清E2、T、血清胰岛素(INS)及空腹血糖(FBG)均明显增高,差异均具有统计学意义(P0.05);PCOS伴2-DM组的血液中INS及FBG浓度均高于PCOS组,差异有统计学意义(P0.05);量子点荧光标记法与免疫组化法结果均显示大鼠卵巢组织中有HSP70的表达,颗粒细胞中表达较多,主要为胞质表达,HSP70的表达趋势为正常组PCOS组PCOS伴2-DM组,HSP70表达量各组间均有统计学差异(P0.05)。结论大鼠卵巢中存在HSP70的表达,且在正常组、PCOS组及PCOS伴2-DM组间存在差异;HSP70在各组间的差异表达可能与PCOS及PCOS伴2-DM的发病机制有关。     

脂联素在多囊卵巢综合征中作用机制的进展

多囊卵巢综合征(PCOS)是育龄期女性最常见的生殖内分泌疾病,主要特征为排卵功能障碍、卵巢多囊样改变、高雄激素血症。PCOS的临床特征具有复杂性和异质性,其发生发展与脂肪组织功能失常密切相关。脂联素是脂肪组织来源的脂肪因子,目前多项研究显示,在PCOS患者及DHEA诱导的PCOS大鼠模型中脂联素的水平显著降低,而脂联素水平与肥胖、胰岛素抵抗、炎症等密切相关。本文主要从激素合成、代谢、炎症等方面阐述脂联素在PCOS发生发展过程中的分子机制,以期为PCOS的诊断和治疗提供一定参考。     

PCOS患者抗苗勒管激素水平与胰岛素抵抗及生殖激素水平的相关性研究

目的探讨多囊卵巢综合征(PCOS)患者血清抗苗勒管激素(AMH)水平与胰岛素抵抗(IR)及生殖激素水平的相关性。方法选取2017年1月至2020年2月在东莞东华医院生殖医学科就诊的PCOS患者62例,根据患者是否存在胰岛素抵抗,分为胰岛素抵抗组(HOMA-IR>2.1,PCOS-IR组,34例)和非胰岛素抵抗组(HOMA-IR<2.1,PCOS-NIR组,28例);选择同时期在同院行健康体检的30例正常女性为对照组。测定所有研究对象的血清生殖激素(AMH、FSH、LH、E2、T、PRL、P)水平,以及硫酸脱氢表雄酮(DHEA)、性激素结合球蛋白(SHBG)及空腹血糖(GLU)空腹胰岛素(FIN)水平等指标,统计分析组间各指标的差异;采用Spearman相关分析分析AMH水平与稳态模型胰岛素抵抗指数(HOMA-IR)的关系。结果3组间平均年龄、体重指数(BMI)及血清FSH、P、PRL、SHBG及DHEA水平均无统计学差异(P>0.05)。与对照组比较,PCOS组(包括PCOS-IR组和PCOS-NIR组)血清AMH、LH及T水平显著升高(P<0.05);与PCOS-NIR组比较,PCOS-IR组FIN[(20.31±12.71)mU/L vs.(5.69±1.98)mU/L]、GLU[(5.58±1.98)mmol/L vs.(4.89±1.98)mmol/L]和HOMA-IR[3.7(2.42,7.09)vs.1.28(0.84,1.63)]显著升高(P<0.05)。相关性分析结果显示,PCOS患者AMH水平与LH水平(r=0.403,P=0.001)及T水平(r=0.403,P=0.000)呈正相关,与FSH水平呈负相关(r=-0.253.P=0.044),而与年龄、BMI、E 2、P、PRL、FIN、GLU、SHBG、DHEA及HOMA-IR不存在显著相关(P>0.05)。结论PCOS患者血清AMH水平高于正常女性,其原因与高雄激素密切相关;PCOS患者血清AMH水平与胰岛素抵抗无相关性。     

Gene Expression of Leptin, Resistin, and Adiponectin in the White Adipose Tissue of Obese Patients with Non-Alcoholic Fatty Liver Disease and Insulin Resistance

Background: Adipose tissue is an active endocrine organ that secretes a variety of metabolically important substances including adipokines. These factors affect insulin sensitivity and may represent a link between obesity, insulin resistance, type 2 diabetes (DM), and nonalcoholic fatty liver disease (NAFLD). This study uses real-time polymerase chain reaction (PCR) quantification of mRNAs encoding adiponectin, leptin, and resistin on snap-frozen samples of intra-abdominal adipose tissue of morbidly obese patients undergoing bariatric surgery. Methods: Morbidly obese patients undergoing bariatric surgery were studied. Patients were classified into two groups: Group A (with insulin resistance) (N=11; glucose 149.84 ± 40.56 mg/dL; serum insulin 8.28 ± 3.52 μU/mL), and Group B (without insulin resistance) (N=10; glucose 102.2 ± 8.43 mg/dL; serum insulin 3.431 ± 1.162 μU/mL). Results: Adiponectin mRNA in intra-abdominal adipose tissue and serum adiponectin levels were significantly lower in Group A compared to Group B patients (P<0.016 and P<0.03, respectively). Although serum resistin was higher in Group A than in Group B patients (P<0.005), resistin gene expression was not different between the two groups. Finally, for leptin, neither serum level nor gene expression was different between the two groups. Serum adiponectin level was the only predictor of nonalcoholic steatohepatitis (NASH) in this study (P=0.024). Conclusions: Obese patients with insulin resistance have decreased serum adiponectin and increased serum resistin. Additionally, adiponectin gene expression is also decreased in the adipose tissue of these patients. This low level of adiponectin expression may predispose patients to the progressive form of NAFLD or NASH.     

血清lncRNA MEG3的表达与多囊卵巢综合征患者胰岛素抵抗的关系

目的 探讨长链非编码RNA(lncRNA)人类母系表达基因3(MEG3)的表达与多囊卵巢综合征(PCOS)患者胰岛素抵抗(IR)的关系.方法 选取2018年7月至2020年8月本院收治的123例PCOS患者为研究对象进行前瞻性分析,根据胰岛素抵抗指数(HOMA-IR)水平分为IR组(n=54)和非IR组(n=69),另...     

Insulin and Metformin Regulate Circulating and Adipose Tissue Chemerin

OBJECTIVE

To assess chemerin levels and regulation in sera and adipose tissue from women with polycystic ovary syndrome (PCOS) and matched control subjects.

RESEARCH DESIGN AND METHODS

Real-time RT-PCR and Western blotting were used to assess mRNA and protein expression of chemerin. Serum chemerin was measured by enzyme-linked immunosorbent assay. We investigated the in vivo effects of insulin on serum chemerin levels via a prolonged insulin-glucose infusion. Ex vivo effects of insulin, metformin, and steroid hormones on adipose tissue chemerin protein production and secretion into conditioned media were assessed by Western blotting and enzyme-linked immunosorbent assay, respectively.

RESULTS

Serum chemerin, subcutaneous, and omental adipose tissue chemerin were significantly higher in women with PCOS (n = 14; P < 0.05, P < 0.01). Hyperinsulinemic induction in human subjects significantly increased serum chemerin levels (n = 6; P < 0.05, P < 0.01). In adipose tissue explants, insulin significantly increased (n = 6; P < 0.05, P < 0.01) whereas metformin significantly decreased (n = 6; P < 0.05, P < 0.01) chemerin protein production and secretion into conditioned media, respectively. After 6 months of metformin treatment, there was a significant decrease in serum chemerin (n = 21; P < 0.01). Importantly, changes in homeostasis model assessment–insulin resistance were predictive of changes in serum chemerin (P = 0.046).

CONCLUSIONS

Serum and adipose tissue chemerin levels are increased in women with PCOS and are upregulated by insulin. Metformin treatment decreases serum chemerin in these women.Polycystic ovary syndrome (PCOS), a common endocrinopathy affecting 5–10% of women in the reproductive age, is characterized by menstrual dysfunction and hyperandrogenism and is associated with insulin resistance and pancreatic β-cell dysfunction, impaired glucose tolerance (IGT), type 2 diabetes, dyslipidemia, and visceral obesity (1,2). The consequent hyperinsulinemia is more prevalent in lean and obese women with PCOS when compared with age- and weight-matched normal women (3).The metabolic syndrome is associated with excessive accumulation of central body fat. As well as its role in energy storage, adipose tissue produces several hormones and cytokines termed ‘adipokines’ that have widespread effects on carbohydrate and lipid metabolism. They appear to play an important role in the pathogenesis of insulin resistance, diabetes, and atherosclerosis (4). Furthermore, it is apparent that accumulation of visceral adipose tissue poses a greater cardiometabolic risk than subcutaneous adipose tissue (5) as removal of visceral rather than subcutaneous adipose tissue has been shown to improve insulin sensitivity (6). Moreover, differences in gene expression of adipocyte-secreted molecules (adipokines) suggest that there are inherent adipose tissue depot–specific differences in the endocrine function of adipose tissue. In relation to this, we have published data on the increased levels of vaspin in women with PCOS (7); vaspin is a recently described adipokine mainly formed in human visceral adipose tissue that has insulin-sensitizing effects (8).Recently, Bozaoglu et al. (9) reported chemerin as a novel adipokine, circulating levels of which significantly correlated with BMI, circulating triglycerides, and blood pressure, features of the metabolic syndrome. In addition, chemerin or chemerin receptor knockdown impaired differentiation of 3T3-L1 cells and attenuated the expression of adipocyte genes involved in glucose and lipid homeostasis (10).With the aforementioned in mind and the fact that there is no literature with regards to chemerin in human adipose tissue and its regulation, in study 1, we assessed circulating chemerin as well as mRNA expression and protein levels of chemerin in subcutaneous and omental adipose tissue depots in women with PCOS against age, BMI, and waist-to-hip ratio (WHR) in matched control subjects. Furthermore, we studied the in vivo (study 2) and ex vivo effects of insulin on circulating chemerin levels via a prolonged insulin-glucose infusion in humans and primary adipose tissue explant cultures, respectively. In study 3 we studied the effects of metformin therapy, widely used in the treatment of PCOS in women, on circulating chemerin levels in tandem with associated changes to clinical, hormonal, and metabolic parameters in the same cohort of PCOS in women. Additionally, we studied the ex vivo effects of metformin and steroid hormones in human primary adipose tissue explants.     

不同配方肠外营养对肝硬化大鼠生长激素/胰岛素样生长因子-1轴的影响

目的探讨不同配方肠外营养对肝硬化大鼠肝部分切除术后生长激素/胰岛素样生长因子-1轴的影响。方法正常大鼠作为对照组,肝硬化大鼠随机分为肝硬化术前组,肝硬化肝部分切除术后1 d组,术后行Novamin肠外营养5 d组,术后行Hepa肠外营养5 d组,各组n=6。测大鼠肝功能、血糖及血清GHI、GF-1I、GFBP-3水平,用RT-PCR法检测肝ALBmRNAI、GF-1 mRNA、IG-FBP-3mRNA的表达,肝组织行Ki67免疫组化染色。结果Hepa组肠外营养5 d后血清ALT、ALP、GH分别为(103±23)IU/L(、571±92)IU/L、(1.55±0.12)ng/ml,均比Novamin组明显降低,而血清IGF-1I、GFPB-3分别为(966.4±54.7)ng/ml(、6.9±0.2)ng/ml,均明显升高,肝ALBmRNA、IGF-1mRNAI、GFBP-3mRNA表达水平分别为(1.24±0.06)、(0.85±0.00)、(0.69±0.02),也明显升高,但肝Ki67指数(4.8%±0.3%vs 4.4%±0.4%)却无显著性差异。血清IGF-1I、GFPB-3与血清AST、ALT、ALP水平呈负相关,与血清ALB呈正相关。结论肝硬化大鼠不同配方肠外营养均可反映在生长激素/胰岛素样生长因子-1轴的变化,检测血清IGF-1,IGFBP-3水平有助于营养素的选择。     

雄激素致高胰岛素与高雄激素性无排卵大鼠模型

给9日龄 SD 雌性大鼠注射丙酸睾丸酮造成雄激素致不孕大鼠(ASR),分别观察卵巢形态、血液及组织匀浆激素含量、糖耐量和血胰岛素水平以及卵泡膜和卵巢间质细胞在体外不同刺激状态下(空白、加胰岛素、加 hCG、加胰岛素+hCG)的 T 含量。结果发现:(1)卵巢体积缩小,呈多囊性改变,无黄体;(2)垂体 LH 含量比对照组降低(P<0.01),肾上腺及卵巢中 T、E_2 含量明显升高(分别为P<0.05及P<0.01);(3)糖耐量下降,胰岛素水平显著升高(分别为 P<0.01及 P<0.05);(4)卵泡膜和卵巢间质细胞体外培养 T 含量明显高于对照组(P<0.001),在 hCG 协同作用下胰岛素可使 ASR 及正常大鼠卵巢 T 含量明显增加(P<0.01)。提示雄激素致不孕大鼠可作为高胰岛素和高雄激素性无排卵的动物模型。     

多囊卵巢综合征青年患者血清脂联素、胰岛素抵抗关系的研究

目的探讨多囊卵巢综合征（PCOS）青年患者血清脂联素（APN）、抵抗素（RST）水平与胰岛素抵抗（1R）的关系。方法PCOS组为38例青年PCOS患者,对照组为27例健康女性,两组中根据体重指数（BMI）分为肥胖组BMI（≥25kg／m^2）和非肥胖组（BMI〈25kg／m^2）。在月经第3～5天晨（PCOS闭经者B超检查无优势卵泡当天）留空腹血。采用酶联免疫吸附法（ELISA）测定血清APN和RST浓度,葡萄糖氧化酶法测定血糖浓度,化学发光法测定胰岛素浓度,根据后两者计算胰岛素敏感指数（ISI）。结果（1）肥胖组与非肥胖组空腹血糖水平比较,差异无统计学意义（P〉0．05）;（2）肥胖组与非肥胖组中,PCOS组的空腹胰岛素水平分别显著高于对照组（P〈0．05）;（3）肥胖组中,PCOS组血清APN和ISI水平显著低于对照组,血清RST水平显著高于对照组（P〈0．05）;（4）非肥胖组中,PCOS组血清APN和ISI水平显著低于对照组,血清RST水平显著高于对照组（P〈0．05）。结论（1）与对照组相比,青年PCOS患者血清中APN水平较低,RST水平较高,其中PCOS肥胖患者尤为明显。（2）青年PCOS患者血清中APN水平的下降和RST水平的升高可能与胰岛素敏感性及IR相关。     

A correlation study of the expression of resistin and glycometabolism in muscle tissue after traumatic brain injury in rats

Objective： To investigate the expression pattern of resistin （RSTN） in skeletal muscle tissue and its influence on glycometabolism in rats with traumatic brain injury （TBI）. Methods： Seventy-eight SD rats were randomly divided into traumatic group （n=36）, RSTN group （n=36） and sham operation group （n=6）. Fluid percussion TBI model was developed in traumatic and RSTN groups and the latter received additional 1 mg RSTN antibody treatment for each rat. At respectively 12 h, 24 h, 72 h, 1 w, 2 w, and 4 w after operation, venous blood was collected and the right hind leg skeletal muscle tissue was sampled. We used real-time PCR to determine mRNA expression of RSTN in skeletal muscles, western blot to determine RSTN protein expression and ELISA to assess serum insulin as well as fasting blood glucose （FBG） levels. Calculation of the quantitative insulin sensitivity check index （Q value） was also conducted. The above mentioned indicators and their correction were statistically analyzed. Results： Compared with sham operation group, the RSTN expression in the skeletal muscle as well as serum insulin and FBG levels revealed significant elevation （P〈0.05）, and reduced Q value （P〈0.05） in traumatic group. Single factor linear correlation analysis showed a significant negative correlation between RSTN expression and Q values （P〈0.001） in traumatic group. Conclusion： The expression of RSTN has been greatly increased in the muscular tissue of TBI rats and it was closely related to the index of glycometabolism. RSTN may play an important role in the process of insulin resistance after TBI.