本文選題：雄激素 + 糖耐量受損　； 參考：《南京醫(yī)科大學(xué)》2015年碩士論文

【摘要】：糖尿病是一種由于胰島素絕對(duì)或相對(duì)不足引起的以高血糖為主要特征的代謝性疾病。目前,糖尿病已成為嚴(yán)重威脅人類健康的全球性公共衛(wèi)生問題。糖耐量受損被認(rèn)為是糖尿病的早期表現(xiàn),可定義為前期糖尿病。胰島素抵抗是2型糖尿病的重要特征,也是2型糖尿病發(fā)生發(fā)展的關(guān)鍵因素。過量雄激素導(dǎo)致女性肥胖、胰島素抵抗的現(xiàn)象受到人們的廣泛關(guān)注,而人們對(duì)高雄激素血癥對(duì)于男性糖代謝的影響卻缺乏足夠的重視。同時(shí)現(xiàn)今社會(huì)雄激素濫用的現(xiàn)象日益嚴(yán)重,外源性過量攝入雄激素對(duì)男性機(jī)體糖代謝產(chǎn)生的影響亟需進(jìn)一步探索。我們以SD大鼠為動(dòng)物模型,探討了長(zhǎng)期超生理水平的雄激素對(duì)糖耐量及胰島素敏感性的影響。我們首先借鑒以往研究,以雌性SD大鼠為模型,篩選出合適的激素緩釋管并驗(yàn)證了其體內(nèi)埋植效果,從而確立了合適的造模方法。實(shí)驗(yàn)過程中,我們發(fā)現(xiàn)用醫(yī)用粘合劑制作的激素緩釋管(緩釋管Ⅱ)明顯優(yōu)于木質(zhì)材料封閉兩端的緩釋管(緩釋管Ⅰ),并且證明了緩釋管Ⅱ可在SD大鼠體內(nèi)正常工作�；谝陨蠋c(diǎn),我們用緩釋管Ⅱ構(gòu)建了高DHT血癥雄性大鼠模型,并且首次發(fā)現(xiàn)長(zhǎng)期(3個(gè)月,3 m)超生理濃度DHT可導(dǎo)致雄性SD大鼠糖耐量受損。結(jié)合胰島素耐量實(shí)驗(yàn)及原代胰島GSIS(Glucose-stimulated insulin secretion,葡萄糖刺激胰島素分泌)功能檢測(cè)等實(shí)驗(yàn),我們發(fā)現(xiàn)其糖耐量受損可能是DHT以間接方式損傷胰島β細(xì)胞功能造成的。綜上所述,長(zhǎng)期(3 m)超生理濃度DHT可引起雄性SD大鼠糖耐量受損及胰島β細(xì)胞功能障礙。本研究將有助于加深人們對(duì)雄激素副作用的認(rèn)識(shí),并對(duì)雄激素濫用者起到一定警醒作用。
[Abstract]:Diabetes is a metabolic disease characterized by hyperglycemia due to absolute or relative deficiency of insulin. At present, diabetes has become a serious threat to human health global public health problems. Impaired glucose tolerance is considered an early manifestation of diabetes and can be defined as prediabetes. Insulin resistance is an important feature of type 2 diabetes and a key factor in the development of type 2 diabetes. Excessive androgen leads to obesity and insulin resistance in women. However, the effect of hyperandrogenemia on glucose metabolism in men is not paid enough attention to. At the same time, the phenomenon of androgen abuse is becoming more and more serious, and the effect of exogenous excessive intake of androgen on glucose metabolism of male body needs to be further explored. We used SD rats as an animal model to study the effects of long-term hyperphysiological androgen on glucose tolerance and insulin sensitivity. Based on the previous studies, we selected suitable steroid sustained-release tubes for female SD rats, and verified the implantation effect in vivo, thus establishing a suitable modeling method. In the course of the experiment, we found that the hormone sustained-release tube (鈪，

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