Thyroid function in male infertility.

摘要: Thyroid gland, previously supposed not tohave any impact on spermatogenesis andmale fertility, are now being recognized ashaving important role in male reproduc-tive functions. Most of the studies theeffectof thyroidhormonesonmalefertilitywereconductedbetweentheyears1970and2000 (1). The effects thyroid hormonealterationsonthereproductivesystemhavebeen studied extensively human sub-jects and animal models that have gener-ally shown changes from normal thy-roid function resulted decreased sexualactivity fertility (2,3). underly-ing mechanisms,however,are constantthroughout all species, results fromdifferent disagree (4).In rats rendered thyrotoxic by T4resulted serum gonadotropinlevels (5), decrease total lipids, cho-lesterol, phospholipids testes, andsynthesize increased amounts testos-terone(6).Inimmaturemalemiceagedlessthan 4weeks,the administration slightlysupra-physiological T4 doses ina tendency toward early maturation andshortening development period. Con-versely, larger TH indecreased testes weights seminal vesi-cles, both mice rabbits (3). Directeffects minimal oxygenconsumption when T4was present testicular slice incubations(7). Finally, spermato-genesis conflicting (8), but it wouldappear does exert a direct effecton mature or rams(9). In rats, T3 affects testis maturation,and receptor (TR) type-1 (TR-1)expression rats’ (10,11). Maxi-mal Sertoli cell proliferation coincides withmaximal binding capacity testis, sug-gesting main target action istheSertolicell.However,T3alsoplaysasig-nificant differentiation semi-niferous epithelium,and rodentshave is an factorin Leydig cells. presenceof necessary to initiate differentiationof mesenchymal cells into progeni-torcells,andT3worksinconcertwithotherhormones [luteinizing hormone (LH) andIGF-I] promote development(12). Data other species (suchas deer, sheep, cattle, birds, mink) alsosuggest component neu-roendocrine system regulates seasonalcycles reproductive activity (13). Theunderlying mechanisms postulate T3triggers cessation reproduction at theend season becausecirculating levels deer rise thetime seasonal transition non-breeding state thyroidectomy resultsin absence regression ofthetestis(14,15).Hypothyroidisminducedor occurring soon after birth was associ-ated with marked sexual anddevelopment delays animals (16). Ratsmade hypothyroid transiently propy-lthiouracil (PTU) showeda size, retardation inSertoli differentiation, prolonga-tion time (17).When became older returnedto euthyroid status, there increaseintestissize,Sertolicellnumber,andspermproduction (18). whereexperimental hypothyroidism andrams left untreated for more than1month, arrest sexualmaturity, testosterone concen-tration as well libido andejaculate (6,19). It would therefore appearthat immature,but mature, testis. Pekary Sat-tin (20) showed hypothyroidismand castration reduced TRH (20).The two most common types thyroiddiseases hyper-thyroidism. Studies assessing ofhypo- hyperthyroidism infer-tility also been conducted humansubjects. Hypothyroidism may result sex bindingglobulin (SHBG) decreasein levels, wellas LH folliclestimulating (FSH) (21). Incases prolonged pre-pubertal hypothy-roidism due drop FSH lev-els, cells, respec-tively less stimulated differentiateinto negatively affecting sper-matogenesis. This increases number ofcells decreases num-ber Thus, patients withhypothyroidism, size isobserved along significant inmature germ within seminifer-ous tubules (22,23). Fortunately, very rare males anoccurrence rate only 0.1% gen-eral population Among studieson subjects, Corrales Hernandezet al. (24) analyzed blood semen sam-ples primary (24). study concluded thathypothyroidism adversely affected semenquality compromising volumeand progressive sperm motility. Krassas