Type 2 diabetes touches young subjects of reproductive age in epidemic proportion. This study assesses glucose, total InsulinT, Insulin2 and insulin receptor subunits α and β in testis during mouse development then, in the spontaneously type 2 diabetes models associated with infertility db/db and ob/ob mice. IR-β and α were also assessed in spermatozoa (SPZ), anterior pituitary (AP) and serum. Serum and tissue glucose were measured with enzymatic colorimetric assays and InsulinT and Insulin2 by ELISAs in serum, interstitial tissue- (ITf) and seminiferous tubule (STf) fractions in14- > 60-day-old normal and db/db, ob/ob and wild type (WT) mice. IR subunits were assessed by immunoblotting in tissues and by immunoprecipitation followed by immunoblotting in serum. Development: Glucose increased in serum, ITf and STf. InsulinT and Insulin2 dropped in serum; both were higher in STf than in ITf. In > 60-day-old mouse ITf, insulinT rose whereas Insulin2 decreased; InsulinT and Insulin2 rose concurrently in STf. Glucose and insulin were high in > 60-day-old ITf; in STf high insulin2 accompanied low glucose. One hundred ten kDa IR-β peaked in 28-day-old ITf and 14-day-old STf. One hundred thirty five kDa IR-α was high in ITf but decreased in STf. Glucose escalated in db/db and ob/ob sera. Glucose doubled in ITf while being halved in STf in db/db mice. Glucose significantly dropped in db/db and ob/ob mice spermatozoa. InsulinT and Insulin2 rose significantly in the serum, ITf and STf in db/db and ob/ob mice. One hundred ten kDa IR-β and 135 kDa IR-α decreased in db/db and ob/ob ITf. Only 110 kDa IR-β dropped in db/db and ob/ob STf and AP. One hundred ten kDa IR-β fell in db/db and ob/ob SPZ. One hundred ten kDa sIR-α rose in the db/db and ob/ob mouse sera. Insulin regulates glucose in tubules not in the interstitium. The mouse interstitium contains InsulinT and Insulin2 whereas tubules contain Insulin2. Decreased 110 kDa IR-β and 135 kDa IR-α in the db/db and ob/ob interstitial tissue suggest a loss of active receptor sites that could alter the testicular cell insulin binding and response to the hormone. Decreased IR-β levels were insufficient to stimulate downstream effectors in AP and tubules. IR-α shedding increased in db/db and ob/ob mice.

中文翻译：

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正常和自发糖尿病和肥胖的ob / ob和db / db不育小鼠睾丸和垂体中的葡萄糖，胰岛素，胰岛素受体亚基α和β

2型糖尿病的流行比例触及育龄的年轻受试者。这项研究评估了与不育症db / db和ob / ob小鼠相关的自发2型糖尿病模型在小鼠发育过程中睾丸中的葡萄糖，总InsulinT，Insulin2和胰岛素受体亚基α和β。还对精子（SPZ），垂体前叶（AP）和血清中的IR-β和α进行了评估。用酶比色法测定血清和组织葡萄糖，ELISA法测定InsulinT和Insulin2血清，间质组织-（ITf）和生精小管（STf）组分在14-> 60天龄正常和db / db，ob / ob和野生型（WT）小鼠。通过组织中的免疫印迹，免疫沉淀，血清中的免疫印迹评估IR亚基。发展：血清，ITf和STf中的葡萄糖增加。血清中的InsulinT和Insulin2下降；STf均高于ITf。在> 60日龄的小鼠ITf中，胰岛素T升高，而胰岛素2降低；STf中的InsulinT和Insulin2同时上升。> 60天龄ITf中的葡萄糖和胰岛素较高；在STf中，高胰岛素2伴随低葡萄糖。在28天的ITf和14天的STf中有110 kDa的IR-β达到峰值。135 kDaIR-α的ITf较高，而STf则下降。葡萄糖在db / db和ob / ob血清中升高。db / db小鼠的ITf中的葡萄糖加倍，而STf中的葡萄糖减半。db / db和ob / ob小鼠精子中的葡萄糖显着下降。db / db和ob / ob小鼠的血清，ITf和STf中的InsulinT和Insulin2明显升高。db / db和ob / ob ITf降低了110 kDaIR-β和135 kDaIR-α。db / db和ob / ob STf和AP中只有110 kDaIR-β下降。db / db和ob / ob SPZ下降了110 kDaIR-β。db / db和ob / ob小鼠血清中有110 kDasIR-α升高。胰岛素调节小管中而非间质中的葡萄糖。小鼠间质含有InsulinT和Insulin2，而肾小管含有Insulin2。db / db和ob / ob间质组织中110 kDaIR-β和135 kDaIR-α降低，表明活性受体位点的丢失可能改变睾丸细胞胰岛素的结合和对激素的反应。降低的IR-β水平不足以刺激AP和肾小管的下游效应子。db / db和ob / ob小鼠的IR-α脱落增加。小鼠间质含有InsulinT和Insulin2，而肾小管含有Insulin2。db / db和ob / ob间质组织中110 kDaIR-β和135 kDaIR-α降低，表明活性受体位点的丢失可能改变睾丸细胞胰岛素的结合和对激素的反应。降低的IR-β水平不足以刺激AP和肾小管的下游效应子。db / db和ob / ob小鼠的IR-α脱落增加。小鼠间质含有InsulinT和Insulin2，而肾小管含有Insulin2。db / db和ob / ob间质组织中110 kDaIR-β和135 kDaIR-α降低，表明活性受体位点的丢失可能改变睾丸细胞胰岛素的结合和对激素的反应。降低的IR-β水平不足以刺激AP和肾小管的下游效应子。db / db和ob / ob小鼠的IR-α脱落增加。