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Kisspeptin in Male Hypogonadism

Kisspeptin levels in idiopathic hypogonadotropic hypogonadism diagnosed male patients and its relation with glucose-insulin dynamic

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Pages 991-994 | Received 17 Dec 2015, Accepted 14 Jul 2016, Published online: 10 Sep 2016
 

Abstract

Male hypogonadism is defined as the deficiency of testosterone or sperm production synthesized by testicles or the deficiency of both. The reasons for hypogonadism may be primary, meaning testicular or secondary, meaning hypothalamohypophyseal. In hypogonadotropic hypogonadism (HH), there is indeficiency in gonadotropic hormones due to hypothalamic or hypophyseal reasons. Gonadotropin-releasing hormone (GnRH) is an important stimulant in releasing follicular stimulant hormone (FSH), mainly luteinizing hormone (LH). GnRH omitted is under the effect of many hormonal or stimulating factors. Kisspeptin is present in many places of the body, mostly in hypothalamic anteroventral periventricular nucleus and arcuate nucleus. Kisspeptin has a suppressor effect on the metastasis of many tumors such as breast cancer and malign melanoma metastases, and is called “metastin” for this reason. Kisspeptin is a strong stimulant of GnRH. In idiopathic hypogonadotropic hypogonadism (IHH) etiology, there is gonadotropic hormone release indeficiency which cannot be clearly described.

A total of 30 male hypogonatropic hypogonadism diagnosed patients over 30 years of age who have applied to Haydarpasa Education Hospital Endocrinology and Metabolic Diseases Service were included in the study. Compared to the control group, the effect of kisspeptin on male patients with hypogonatropic hypogonadism and on insulin resistance developing in hypogonadism patients was investigated in our study.

A statistically significant difference was detected between average kisspeptin measurements of the groups (p < 0.01). Kisspeptin measurement of the cases in the patient group were detected significantly high. No statistically significant relation was detected among kisspeptin and LH/FSH levels. Although a positive low relation was detected between kisspeptin measurements of patient group cases and homeostasis model assessment of insulin resistance (HOMA-IR) measurements, this relation was statistically insignificant. When the patient and control groups were compared for HOMA-IR, no statistically significant difference was detected.

The reason for high kisspeptin levels in the patient group compared to the control group makes us consider that there may be a GPR54 resistance or GnRH neuronal transfer pathway defect. When patients and control groups were compared for HOMA-IR, the difference was not statistically significant. It is considered that kisspeptin is one of the reasons for hypogonatropic hypogonadism and has less effect on insulin resistance.

Chinese abstract

男性性腺功能减退症是指雄激素分泌缺乏和(或)睾丸合成精液量不足。性腺功能减退的原因可分为原发性: 睾丸性, 或者继发性: 下丘脑垂体性。在低促性腺激素性性腺功能减退症 (HH) 的患者, 由于下丘脑或者垂体的原因导致促性腺激素水平不足。促性腺激素释放激素 (GnRH) 是卵泡刺激素 (FSH) 和主要的黄体生成素 (LH) 的重要兴奋剂。GnRH的缺失是受多种激素或刺激因子的影响。Kisspeptin出现在身体的多个地方, 大部分在下丘脑前腹侧面室旁核和弓状核。Kisspeptin可以抑制很多肿瘤例如乳腺癌和恶性黑色素瘤的的转移, 因此又称为转移抑素。Kisspeptin是GnRH的强兴奋剂, 在特发性低促性腺激素性性腺功能减退症 (IHH) 的病因学中, 促性腺激素释放不足不能被清楚的描述。

我们的研究纳入了30个30岁以上男性低促性腺激素性性腺功能减退症的确诊患者, 他们已经申请了Haydarpasa Education医院内分泌和代谢疾病的服务。在我们的研究中, kisspeptin对男性低促性腺激素性性腺功能减退症和对性腺机能减退患者胰岛素抵抗进展的影响与照组进行了比较。在每组之间平均Kisspeptin测量结果有统计学差异 (P<0.01) 。在患者组Kisspeptin测量结果显著升高。Kisspeptin和LH/FSH水平无显著的统计学相关性。虽然Kisspeptin测量结果在患者组病例和胰岛素抵抗的稳态模型评价(HOMA-IR)中比较有较低的相关性, 但是这种相关性没有统计学意义。患者组和对照组在HOMA-IR中无统计学差异。

我们认为与对照组相比, 患者组高Kisspeptin水平的原因可能由于GPR54抵抗或者GnRH神经传导通路缺陷。患者组与对照组在HOMA-IR的比较没有统计学意义。因此认为Kisspeptin是低促性腺激素性性腺功能减退症的原因之一并且对胰岛素抵抗有较小的影响。

Declaration of interest

All authors declare no conflict of interest.

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