diabetes mellitus and impairment of male reproductive function: role of hypothalamus pituitary testicular axis and reactive oxygen species

abstract diabetes mellitus (dm) is one of the greatest public health threats in modern societies. although during a few years it was suggested that dm had no significant effect in male reproductive function, this view has been challenged in recent years. from a clinical perspective, the evaluation of semen parameters, as well as spermatozoa deoxyribonucleic acid (dna) integrity, are often studied due to their direct implications in natural and assisted conception. testicular cells have their own glucose sensing machinery that react to hormonal fluctuations and have several mechanisms to counteract hyper- and hypoglycaemic events. moreover, the metabolic cooperation between testicular cells is crucial for normal spermatogenesis. sertoli cells (scs), which are the main components of blood–testis barrier, are not only responsible for the physical support of germ cells but also for lactate production that is then metabolized by the developing germ cells. any alteration in this tied metabolic cooperation may have a dramatic consequence in male fertility potential. diabetes-related oxidative stress may also be the trigger for many alterations on sexual function (poor semen quality, erectile and testicular dysfunction, impotence, decreased fertility potential and retrograde ejaculations), which can also include decreased testicular mitochondrial function. in addition, diabetic men have decreased serum testosterone due to impaired leydig cell function which is accompanied by low lh and fsh; the inability of the pituitary gland to respond appropriately to a decline in testosterone implying central effect of high serum glucose on the interaction between the nervous and endocrine system. therefore, this review article highlights the impact of diabetes and associated, oxidative stress with reference to hypothalamus pituitary testicular axis.