Diabetes Mellitus and Infertility: Different Pathophysiological Effects in Type 1 and Type 2 on Sperm Function.
Diabetes Mellitus and Infertility: Different Pathophysiological Effects in Type 1 and Type 2 on Sperm Function.
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DOI：
10.3389/fendo.2018.00268
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发表时间：
2018
影响因子：
5.2
通讯作者：
Calogero AE
中科院分区：
文献类型：
--
作者：
Condorelli RA;La Vignera S;Mongioì LM;Alamo A;Calogero AE
虽然育龄期糖尿病患者亚不育的患病率是已知的，但糖尿病（DM）导致男性不育的机制尚未完全解释。这种不利影响是通过多种机制实现的，包括睾丸前、睾丸和睾丸后发病时刻，并且由于糖尿病类型、疾病持续时间和血糖代谢补偿，1型糖尿病（DM 1）和2型糖尿病（DM 2）患者可能不同。本研究的目的是评估糖尿病是否可以被认为是不孕症的危险因素，考虑到DM 1和DM 2对精子功能的病因学差异。我们招募了38名DM 1患者和55名DM 2患者，他们的特发性不孕病史>12个月，以及100名健康生育者。通过光学显微镜和流式细胞术评价了以下结局：精子功能（通过常规和生物功能精子参数）和泌尿生殖道感染/炎症体征（通过精子白细胞浓度和氧化应激指数）。此外，与对照组相比，DM 1和DM 2患者进行了男性学评价（通过附睾-附睾超声评价，血清总睾酮，LH和FSH测量）。糖尿病患者表现出更高的风险成为不孕症和损害的病理生理机制是不同的DM 1和DM 2。糖尿病患者精子常规参数较对照组差（P < 0.05）。DM 2引起炎症，氧化应激增加，导致精子活力降低和精子DNA片段化增加。DM 1改变附睾排尿，导致射精量低和线粒体损伤，导致精子活力降低。这些发现和证据支持DM可被视为男性不育的原因的论点，表明DM 2中糖尿病疾病的预防和DM 1中精液参数的随访可预防这些类别患者的生育力下降。
Although the prevalence of sub-infertility in diabetic patients in childbearing age is known, the mechanisms by which diabetes mellitus (DM) causes male infertility are not completely explained. This detrimental effect is achieved with a variety of mechanisms that include pre-testicular, testicular, and post-testicular pathogenetic moments and can be different in type 1 diabetes mellitus (DM1) and type 2 diabetes mellitus (DM2) patients because of type of diabetes, duration of disease, and glycemic metabolic compensation. Aim of this study was to evaluate whether diabetic disease can be considered a risk factor for infertility considering the etiopathogenetic differences between DM1 and DM2 on sperm function. We enrolled 38 DM1 patients and 55 DM2 patients with idiopathic infertility history >12 months, and 100 healthy fertile subjects. The following outcomes were evaluated in optical microscopy and flow cytometry: sperm function (by conventional and biofunctional sperm parameters) and signs of urogenital infection/inflammation (by sperm leukocyte concentrations and indices of oxidative stress). Moreover, an andrological evaluation (by didymo-epididymal ultrasound evaluation, serum total testosterone, LH, and FSH measurements) was performed in DM1 and DM2 patients compared to controls. Diabetic patients showed a higher risk of becoming infertile and the pathophysiological mechanisms of damage were different in DM1 and DM2. Conventional sperm parameters of diabetic patients are worse than controls (p < 0.05). The DM2 caused an inflammatory condition with increased oxidative stress resulting in decreased sperm vitality and increased sperm DNA fragmentation. DM1 altered epididymal voiding causing low ejaculate volume and mitochondrial damage resulting in decreased sperm motility. These findings and evidences support the contention that DM could be regarded as cause of male infertility suggesting that the prevention of diabetic disease in DM2 and the follow-up of seminal parameters in DM1 could prevent fertility decline in these categories of patients.