Hormones influence life of all animals. Not only they affect physiological changes in organisms, but also impact their behaviour. This work focuses at two main groups of steroid hormones: glucocorticoids and androgens. Glucocortiods are activated in response to stress. Their levels can be measured using non-invasive methods, which have a range of advantages. The main advantage is the feedback-free sample collection for enzyme immunoassay. As the measurement involves metabolites of the hormones rather than the hormones themselves, prior validation of the method is, however, necessary. This work reports on a study aiming to validate non-invasive measurement on the Madagascar Ground Gecko (Paroedura Picta). The validation was based on ACTH challenge test: Synacthen Depot was injected, which should lead to increased blood level of glucocorticoids. The validation, however, was not successful. The measurement did not discover significant increase in the levels of the metabolites of glucocorticoids. In addition, the work focuses on behavioural effects of testosterone, the primary androgen. Hormonal manipulations have been carried out on several male and female specimens. The results have discovered differences in sexual behaviour between control groups. On the other hand, the hormonal manipulations had no...

Den här studien syftar till att undersöka vuxnas erfarenheter av sexuella problem under könsbekräftande behandling med testosteron, samt erfarenheter av samtal om sexuell hälsa inom den könsbekräftande vården. Tidigare forskning har visat att omfattningen av studier på området är bristfälligt. Studien har genomförts med kvalitativ metod och fenomenologisk ansats. Den består av berättelser från sex halvstrukturerade livsvärldsintervjuer som har analyserats med reflexiv tematisk analys. Fyra huvudteman presenteras i resultatanalysen: Nya sexuella kroppar, Nya sexuella känslor, Nya sexuella rum och relationer och Olika vård för lika problem. Resultaten visar att sexuella problem under könsbekräftande behandling är en flytande process där olika individuella, interpersonella och kontextuella faktorer spelar in. Sarah Ahmeds (2006) queera fenomenologi och Jack Halberstams (2005) begrepp queer tid har använts för att identifiera processer av orientering i tid och rum. Resultaten visar även på olika erfarenheter av den könsbekräftande vårdens förmåga att tillgodose behov för sexologiskt stöd samt ett fortsatt behov av forskning och insatser på området. / This study aims to explore adults’ experiences of sexual problems during gender affirming treatment with testosterone, and experiences of conversations about sexual health within gender affirming health care services. Previous research shows that there is a lack of studies on the subject. This study has been conducted with qualitative methods and phenomenological approach. It is constituted by stories from six semi structured interviews which has been analyzed through reflexive thematic analysis. Four themes are presented in the result analysis: New sexual bodies, New sexual feelings, New sexual spaces and relationships and Different care for equal needs. The results show that sexual problems during gender affirming treatment is a fluent process where different individual, interpersonal and contextual factors contribute. Sarah Ahmed’s (2006) queer phenomenology and Jack Halberstam’s (2005) queer time has been used to identify processes of orientation in time and space. The results also show different abilities for gender affirming health care services to meet the needs for support from a sexologist, and a need for future research on the subject.

Les récepteurs Erythropoietin-producing hepatocyte (EPH) constituent la plus grande famille de récepteurs à activité tyrosine kinase transmembranaires. Leur activité kinase peut être induite par leurs ligands, les éphrines (EFN). Une fois activés, ces récepteurs sont impliqués dans la régulation de la fonction cellulaire par transduction antérograde ou rétrograde du signal EPH-EFN. Au cours de la dernière décennie, nos études ont démontré que les EPH / EFN jouent un rôle important dans la régulation de la pression artérielle par la modulation de la contractilité des cellules musculaires lisses vasculaires (VSMC). EPHB6, EFNB1 et EFNB3 ont un effet négatif sur la contractilité des VSMC et la pression artérielle, tandis que EPHB4 et EFNB2 montrent un effet positif. La famille EPH / EFN est donc un nouveau système yin et yang qui ajuste finement l'homéostasie de la pression artérielle. Nous avons également constaté que les catécholamines urinaires de 24 h sont réduites chez les souris mâles EPHB6 knockout (KO), suggérant que l’EPHB6 régule la pression artérielle non seulement via les VSMC mais aussi par la sécrétion de catécholamine (CAT). La régulation de CAT par l’EPHB6 dépend de la testostérone car (1) les niveaux réduits de CAT ne sont pas observés chez les souris femelles EPHB6 KO ; et (2) la castration chez les souris mâles EPHB6 KO ramène la CAT à des niveaux normaux. Durant ma thèse, nous avons étudié le mécanisme impliqué dans la régulation de la sécrétion et de la synthèse des catécholamines chez les cellules chromaffines des glandes surrénales (AGCC) par la voie de signalisation de l’EPHB6. En ex vivo, la teneur totale en épinéphrine et la sécrétion d'épinéphrine déclenchée par l'acétylcholine (ACh) sont toutes deux réduites dans les glandes surrénales venant des souris KO mâles mais pas dans celles venant des femelles ou de mâles castrés. Ensuite, nous avons observé une diminution de l’afflux de Ca2+ dépendant de l'ACh dans les AGCC venant des souris mâles EPHB6 KO, ce qui découle de l'effet non-génomique de la testostérone. En appliquant le patch clamping de cellules entières sur les AGCC, nous avons démontré que la diminution d’afflux de Ca2+ dans ces cellules est causée par l’augmentation des courants de potassium à grande conductance activé par le calcium (BK). En utilisant l'enregistrement ampérométrique, nous avons constaté que la sécrétion de CAT par les AGCC est compromise en l'absence d'EPHB6. Nous avons également observé une diminution du désassemblage de la F-actine corticale dans les AGCC venant de souris mâles KO associée à une diminution de l'exocytose des vésicules contenant es catécholamines. Ces deux phénomènes n’ont pas été observés chez les femelles KO ni chez les mâles castrés. Des études complémentaires ont montré que le désassemblage défectueux de la F-actine dans les AGCC est régulé par la signalisation inverse de l'EPHB6 à l'EFNB1 via deux voies de signalisations différentes : la voie du membre A de la famille des homologues Ras (RHOA) et la voie de la tyrosine kinase proto-oncogène de la famille Src (FYN) / proto-oncogène c-ABL / la calponine monooxygénase associée aux microtubules et le domaine LIM contenant 1 (MICAL-1). En outre, nous avons observé que la diminution de la teneur totale en épinéphrine dans la glande surrénale venant des souris mâles KO est causée par une expression altérée de la tyrosine hydroxylase (TH), qui est l’enzyme limitant la vitesse dans la biosynthèse des CAT. L'effet non génomique de la testostérone a également participé dans ce processus. Nous avons révélé que la signalisation inverse d'EPHB6 à EFNB1 contribue à la surexpression de TH dans les AGCC par l’augmentation de son niveau de transcription. La voie en aval de cette signalisation inverse implique la petite famille Rac GTPase 1 (RAC1) / MAP kinase kinase 7 (MKK7) / c-Jun N-terminal kinase (JNK) / proto-oncogène c-Jun / activator protein 1 (AP1) / réponse de croissance précoce 1 (EGR1). Ces travaux démontrent pour la première fois un rôle spécifique de la famille EPH / EFN dans la régulation de la biologie médullaire de la glande surrénale. La signalisation rétrograde d’EPHB6 via EFNB1 régule la synthèse et la sécrétion des catécholamines de concert avec la testostérone dans les AGCC. / Erythropoietin-producing hepatocyte (Eph) receptors are the largest family of cell surface transmembrane receptor tyrosine kinases. Their kinase activity can be activated by their ligands, ephrins (EFNs), and involved in cell function regulation through either EPH-EFN forward or reverse signaling transduction. In the last decade, we have revealed the previously unknown function of EPHs/EFNs in the regulation of blood pressure by modulating the contractility of vascular smooth muscle cells (VSMCs). EPHB6, EFNB1, and EFNB3 have a negative effect on the VSMCs contractility and blood pressure, while EPHB4 and EFNB2 show a positive effect instead. Thus, EPH/EFN family is a novel yin and yang system that finely tunes blood pressure homeostasis. EPHB6 also targets cells responsible for catecholamine (CAT) secretion in addition to the VSMCs, since we found that the 24-h urine catecholamines are reduced in male EPHB6 knockout (KO) mice. This phenotype in EPHB6 KO mice is testosterone-dependent because the reduced CAT levels are not observed in female KO mice; castration in KO male mice reverts the CAT levels to a normal range. In this research, we investigated the mechanism for the regulation of catecholamine secretion and synthesis in adrenal gland chromaffin cells (AGCCs) by EPHB6 signaling. In ex vivo, the total content of epinephrine and the acetylcholine (ACh)-triggered epinephrine secretion were both reduced in the adrenal gland from KO male but not female or castrated mice. Then, we found a reduced ACh-dependent Ca2+ influx in AGCCs from male EPHB6 KO mice, and this effect depended on the non-genomic effect of testosterone. The results of whole-cell patch clamping on AGCCs indicated that the enhanced large-conductance calcium-activated potassium (BK) currents were responsible for the reduced Ca2+ influx in these cells. Using amperometry recording, we found that CAT secretion by AGCCs was compromised in the absence of EPHB6. The cortical F-actin disassembly in AGCCs from KO male but not female or castrated mice was reduced, accompanied by decreased catecholamine vesicle exocytosis. Further study showed such defective F-actin disassembly in AGCCs was regulated by the reverse signaling from EPHB6 to EFNB1 via the Ras homolog family member A (RHOA) and proto-oncogene Src family tyrosine kinase (FYN)/proto-oncogene c-ABL/microtubule-associated monooxygenase calponin and LIM domain containing 1 (MICAL-1) pathways. Further, we observed that the reduced total content of epinephrine in the adrenal gland from male KO mice was caused by impaired expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in CAT biosynthesis. The non-genomic effect of testosterone was also involved in this process. We revealed that the reverse signaling from EPHB6 to EFNB1 contributed to the up-regulation of TH expression in AGCCs by enhancing its transcription. The downstream pathway of this reverse signaling involved Rac family small GTPase 1 (RAC1)/MAP kinase kinase 7 (MKK7)/c-Jun N-terminal kinase (JNK)/ proto-oncogene c-Jun/activator protein 1 (AP1)/early growth response 1 (EGR1). The present research, for the first time, revealed the specific role of the EPH/EFN family on the regulation of the adrenal gland medullary biology. The EPHB6 reverse signaling through EFNB1 in concert with testosterone regulates the catecholamine synthesis and secretion in AGCCs.

Objective: Lower levels of anabolic hormones in older age are well documented. Several studies suggested that low insulin-like growth factor I (IGF-I) or testosterone levels were related to increased mortality. The aim of the present study was to investigate the combined influence of low IGF-I and low testosterone on all-cause mortality in men. Methods and results: From two German prospective cohort studies, the DETECT study and SHIP, 3942 men were available for analyses. During 21,838 person-years of follow-up, 8.4% (n = 330) of men died. Cox model analyses with age as timescale and adjusted for potential confounders revealed that men with levels below the 10th percentile of at least one hormone [hazard ratio (HR) 1.38 (95% confidence-interval (CI) 1.06–1.78), p = 0.02] and two hormones [HR 2.88 (95% CI 1.32–6.29), p < 0.01] showed a higher risk of all-cause mortality compared to men with non-low hormones. The associations became non-significant by using the 20th percentile as cut-off showing that the specificity increased with lower cut-offs for decreased hormone levels. The inclusion of both IGF-I and total testosterone in a mortality prediction model with common risk factors resulted in a significant integrated discrimination improvement of 0.5% (95% CI 0.3–0.7%, p = 0.03). Conclusions: Our results prove that multiple anabolic deficiencies have a higher impact on mortality than a single anabolic deficiency and suggest that assessment of more than one anabolic hormone as a biomarker improve the prediction of all-cause mortality.

<p> The age at which a juvenile female reaches sexual maturity can be modulated by a variety of environmental and social factors. Experiments described in this thesis were designed to enhance the current understanding of the relationships among three variables that influence the onset of sexual maturation in female mice (Mus musculus), including: [1] exposure to dietary phytoestrogens during development, [2] variations in prenatal androgens, and [3] the presence or absence of genetically-unrelated males after weaning. For the first time, age at onset of male-induced female puberty was investigated using non-invasive behavioural and fertility measures. Through enzyme immunoassay procedures, daily output of urinary creatinine, 17P-estradiol, and progesterone was profiled in developing females that were either isolated or exposed to adult males. Uterine and ovarian tissue was also measured in such females, and male exposure was observed to increase reproductive tissue mass and was influenced by prior androgen exposure in interaction with diet and male presence. Male-exposed females fed a diet containing phytoestrogens immediately became sexually receptive when housed directly with males, and they conceived earlier than females in other conditions. Females with longer anogenital distance, which reflects higher in utero androgen exposure, displayed more escape attempts and aggressive posturing in the direct presence of males, especially when they had been housed near males and fed the phytoestrogen-containing diet. Urinary 17P-estradiol was substantially reduced in females raised on the phytoestrogenfree diet. Urinary output of progesterone was not strongly influenced by diet. Maleexposed females ' output of progesterone and 17P-estradiol was more dynamic in comparison to that of isolated females. The size of this effect depended on diet, prior androgen exposure, and whether urinary steroid measures were adjusted by urinary creatinine. Urinary creatinine was elevated by the low phytoestrogen diet and reduced by male exposure. These data suggest that dietary phytoestrogens and in utero androgen exposure interact with presence or absence of males in determining the age at onset of sexual maturity in developing females. </p> <p> A final experiment was designed to examine two components of adult male urine, preputial gland emissions and unconjugated estrogens, that have been posited to act on females to advance reproductive maturation. Intact and preputialectomized males were compared in their output of urinary creatinine, 17~-estradiol, and testosterone, and in their influence on reproductive tissue in juvenile females. Lack of preputial glands did not hinder the capacity of males to induce uterine and ovarian growth in females. Male urinary creatinine was reduced by exposure to juvenile females. Creatinine-adjusted 17~estradiol and testosterone were greater in female-exposed males, regardless of whether the preputial glands were present. Based on these findings and those reported elsewhere, it is probable that male excreted urinary steroids are important in regulating reproductive changes in developing females exposed to males. </p> / Thesis / Doctor of Philosophy (PhD)

Peripheral blood biomarkers can inform clinical care and drug development. Establishing causality between biomarker and disease is often critical for such applications, but epidemiological studies are limited due to biases from confounding and reverse causation. Mendelian randomization analysis leverages random inheritance of genetic variants at conception to mimic properties of randomized studies and estimate unconfounded effects between biomarker and disease, or vice-versa. This thesis demonstrates the utility of Mendelian randomization as a complementary tool to elucidate observational studies, predict drug safety and repurposing opportunities, and improve diagnostic biomarkers for cardiometabolic diseases. First, we characterized the hypothesized relationship between lipoprotein(a) and atrial fibrillation. We demonstrated both observed and genetically predicted lipoprotein(a) levels were associated with higher risk of atrial fibrillation across multiple independent cohorts. Importantly, risk was partly mediated independent of atherosclerotic cardiovascular disease, a known consequence of elevated lipoprotein(a) and itself a risk factor for atrial fibrillation. Next, we explored the lifelong effects of endogenous testosterone across a comprehensive set of 461 health outcomes in 161,268 males from the UK Biobank cohort. Using Mendelian randomization analysis, we found higher testosterone had beneficial effects on body composition and bone mineral density but adverse effects on prostate cancer, androgenic alopecia, spinal stenosis, and hypertension. Finally, we applied Mendelian randomization with the intention of discovering biomarkers caused by disease, which are expected to represent markers of early disease. As a proof-of-concept, we applied this framework to identify biomarkers associated with genetic predisposition to kidney function among 238 biomarkers measured in the ORIGIN trial. We discovered reduced kidney function caused increased trefoil factor 3 and showed its addition to models with known risk factors improved discrimination of incident early-stage chronic kidney disease. Taken together, Mendelian randomization identified biomarkers that warrant further study, with promising implications for screening, prevention, and treatment of different cardiometabolic diseases. / Thesis / Doctor of Philosophy (PhD) / Biological markers associated with disease can inform novel therapeutics or diagnostics but distinguishing causation from correlation is challenging. Mendelian randomization – a technique that leverages random inheritance of genetic variation to infer causality – was used to examine the role of biomarkers in cardiometabolic diseases. First, we implicated lipoprotein(a) as a risk factor for atrial fibrillation that acts independent of atherosclerotic cardiovascular disease. Second, we comprehensively characterized the lifelong effects of testosterone on health outcomes in males, where we found evidence of both beneficial and adverse effects on disease. Finally, we discovered trefoil factor 3 as a diagnostic marker for early-stage chronic kidney disease. Altogether, this thesis demonstrated different applications of Mendelian randomization that showcase its utility as a complementary tool to reveal causal biomarkers, and served to identify biomarkers for cardiometabolic diseases that merit further studies to evaluate their potential benefit on patient care.

Indiana University-Purdue University Indianapolis (IUPUI) / Although peripheral motoneurons are phenotypically endowed with robust regenerative capacity, functional recovery is often suboptimal following peripheral nerve injury (PNI). Research to date indicates that the greatest success in achieving full functional recovery will require the use of a combinatorial approach that can simultaneously target different aspects of the post-injury response. In general, the concept of a combinatorial approach to neural repair has been established in the scientific literature but has yet to be successfully applied in the clinical situation. Emerging evidence from animal studies supports the use of electrical stimulation (ES) and testosterone as one type of combinatorial treatment after crush injury to the facial nerve (CN VII). With the facial nerve injury model, we have previously demonstrated that ES and testosterone target different stages of the regeneration process and enhance functional recovery after facial nerve crush injury. What is currently unknown, but critical to determine, is the impact of a combinatorial treatment strategy of ES and testosterone on functional recovery after crush injury to the sciatic nerve, a mixed sensory and motor spinal nerve which is one of the most serious PNI clinical problems. The results of the present study indicate that either treatment alone or in combination positively impact motor recovery. With regard to molecular effects,single and combinatorial treatments differentially alter the expression of regeneration-associated genes following sciatic nerve crush injury relative to facial nerve injury. Thus, our data indicate that not all injuries equally respond to treatment. Furthermore, the results support the importance of treatment strategy development in an injury-dependent manner and based upon the functional characteristics of spinal vs. cranial nerves.

Malgré le fait que le statut social soit reconnu comme ayant une forte influence sur l’aptitude, les facteurs affectant le statut social et les changements de ce statut demeurent peu connus. De plus, les études sur la dominance ayant un lien avec l’agressivité portent rarement sur des femelles. Nous étudierons ces aspects en utilisant Neolamprologus pulcher, un poisson à reproduction coopérative du lac Tanganyika. La probabilité d’ascension sociale était manipulée sur le terrain et les changements physiologiques et comportementaux, ainsi que le niveau plasmatique de testostérone, associé avec l’ascension à la dominance de femelles subordonnées étaient caractérisés. Le degré de coopération et la masse étaient supérieurs chez les femelles ascendantes par rapport aux femelles non-ascendantes d’un même groupe social. Après une semaine d’ascension sociale, les femelles ascendantes ne différaient pas comportementalement, mais différaient physiologiquement des femelles dominantes. Les femelles dominantes, ascendantes et subordonnées ne différaient pas quant au niveau de testostérone plasmatique. Comprendre les bénéfices des comportements coopératifs pour les subordonnés a longtemps posé un problème évolutif. Nos résultats impliquent que les comportements coûteux métaboliquement peuvent avoir été sélectionnés en améliorant l’aptitude future via l’héritage du territoire et du statut social. De plus, le degré de coopération pourrait être un signal de qualité détecté par les compétiteurs et les collaborateurs. / Although social rank is known to have a strong influence on fitness, factors affecting rank and changes in rank remain poorly understood. In addition, studies of dominance and its relation to aggression rarely focus on females. We address these issues in this study using Neolamprologus pulcher, a cooperatively breeding fish species from Lake Tanganyika. The probability of social ascension was manipulated in the field and the physiological and behavioural changes as well as plasma testosterone level associated with subordinate female ascension were characterized. Both helping effort (degree of cooperation) and body size were greater in ascending versus paired same social group non-ascending females. After one week of social ascension, ascending females did not differ behaviourally but were physiologically different (higher body condition, smaller, lighter) from dominant females. Dominant, ascending females and subordinate females did not differ in plasma testosterone levels. Understanding the benefits of helping behaviour for subordinates has long been an evolutionary challenge and our results imply that this costly metabolic behaviour may have been selected by enhancing future fitness via territory and rank inheritance. Furthermore, helping effort could be a signal of quality detected by both competitors and collaborators.

O líquen escleroso vulvar é uma doença crônica e benigna, porém apresenta um potencial de malignização para o carcinoma de células escamosas de vulva. Foram estudadas trinta doentes com líquen escleroso vulvar, divididas em três grupos, que fizeram uso tópico de propionato de clobetasol a 0,05%, testosterona a 2% e um placebo, para avaliar a evolução dos sintomas e o comportamento das células marcadas com o anticorpo Ki-67 e a proteína p53 antes e após os tratamentos. Observou-se melhora dos sintomas clínicos com o uso do clobetasol e da testosterona, que foi estatisticamente superior ao placebo (p<0,01). Observou-se diminuição significante das células marcadas com Ki-67 após o tratamento das doentes com o clobetasol (p<0,01) e com a testosterona (p<0,02). Enquanto, nas doentes que utilizaram placebo, observou-se um aumento do Ki-67. Em relação à análise das células marcadas com a proteína p53 também observou-se diminuição significante após o tratamento com o clobetasol (p<0,01) e com a testosterona (p<0,01). Enquanto no grupo placebo observou-se um aumento do p53. Quando se compara a variação do p53 entre os grupos clobetasol, testosterona e placebo observou-se uma diminuição do p53 estatisticamente superior (p<0,001) nas doentes que utilizaram clobetasol. Assim, os resultados mostram uma redução dos marcadores celulares após os tratamentos, e com o p53 a diminuição foi estatisticamente maior no grupo que utilizou clobetasol, sugerindo a eficácia desse tratamento / Vulvar Lichen Sclerosus consists of a benign chronic disease, however featuring a malignant potential for vulvar squamous cell carcinoma. The present study targeted 30 patients diagnosed Vulvar Lichen Sclerosus, divided in three groups, and who made topical use of clobetasol propionate at 0.05%, testosterone at 2% and a placebo, so as to assess the evolution of the symptoms and the behavior of the cells marked with antibody Ki-67 and protein p53, before and after the treatments. The administration of clobetasol and testosterone has proven effective in the management of the clinical symptoms, which turned out to be statistically higher than the placebo (p<0.01). The number of cells marked with Ki-67 decreased significantly patients treated with clobetasol (p<0.01) and testosterone (p<0.02), while the number of such cells increased in those patients who made use of the placebo. The number of cells marked with protein p53 also decreased significantly after the treatment with clobetasol (p<0.01) and testosterone (p<0.01), whereas the placebo group revealed an increased p53. When comparing the decrease of the p53 in the clobetasol, testosterone and placebo groups, we noted a decrease of the p53 statistically higher (p<0.001) in patients under clobetasol; suggesting a reduction in the cellular markers after the treatment. As for the p53, the decrease was statistically higher in the group under clobetasol, suggesting the efficacy of the treatment.

A vitamina D é uma molécula versátil que possui ação genômica e não genômica em múltiplas reações dos seus órgãos que possuem a expressão de seu receptor (VDR), inclusive do trato reprodutivo de ambos os sexos, além dos seus clássicos efeitos no metabolismo ósseo, e na homeostase do cálcio e fosfato. Novas evidências a partir de estudos experimentais e com humanos sugerem que a vitamina D está envolvida nas funções dos órgãos reprodutivos masculinos, influenciando na espermatogênese. O objetivo do presente estudo foi avaliar a influência dos níveis séricos de 25(OH)D com os parâmetros de qualidade seminal em homens normozoospérmicos e com alterações nos parâmetros seminais. Nesse estudo retrospectivo, dos 508 pacientes atendidos no período de 2009 até 2017 com todas as dosagens séricas e análise seminal, selecionamos os dados de 260 pacientes que atenderam aos critérios de inclusão, de uma clínica médica de Andrologia da cidade de São Paulo. Eles foram divididos em dois grupos: Grupo normozoospermicos (NZG; N=124) e Grupo com parâmetros Seminais Alterados (SAG; N=136). Foram considerados as dosagens séricas de 25(OH)D, e as variáveis de confusão ambientais, como uso de álcool, tabaco, sedentarismo, índice de massa corporal (IMC), e presença de varicocele. As analises seminais foram realizadas e classificadas de acordo com o manual da OMS 2010, e foram consideradas para o estudo os parâmetros de pH, volume, motilidade total e progressiva, morfologia por OMS e Kruger. Além disso, foram consideradas os exames de Cariótipo e Micro deleção no Cromossomo Y. As análises estatísticas foram realizadas com o SPSS versão 19.0. Correlação de Spearman, Mann-Whitney e um modelo de regressão multivariada foram aplicadas. Significância considerada foi de P <= 0.05. A distribuição das médias dos níveis séricos de 25(OH)D foi significativamente menor nos pacientes do grupo com parâmetros seminais alterados (P =0.016), e foi encontrado uma correlação positiva entre os níveis séricos de 25(OH)D e todos os parâmetros de qualidade seminal analisados, excetos de pH e volume. Foi descrita correlação forte entre 25(OH)D e motilidade total (r=0,225; P =0,001). Os resultados obtidos nesse estudo mostram que os níveis séricos de 25(OH)D possuem uma correlação positiva com os parâmetros de motilidade, concentração e morfologia do espermatozoide, de forma independente. Esses achados indicam que a adequação dos níveis de vitamina D podem ser um importante coadjuvante no tratamento da infertilidade masculina / Vitamin D is a versatile signaling molecule, that targets also male reproductive organs, in addition to the classic effects on bone, calcium and phosphate homeostasis. Accumulating evidence from animal and human studies suggests that it is involved in reproduction functions in both genders. This study aimed to evaluate the vitamin D correlation with semen quality in male with seminal parameters alteration and normozoospermic diagnosis. We selected 260 men (aged 18 to 60 y.o.) from a private andrology reference medical clinic for this observatory study. They were divided in two groups: Normal seminal parameters (NZG N=124) and Abnormal seminal parameters (SAG N=136). 25(OH) vitamin D serum concentration were collected such as lifestyle data available. Semen was analyzed according to WHO 2010 guidelines, ph, volume, motility, concentration, morphology, strict criteria and sperm functional tests were performed (ROS, CK, beads). In addition, karyotype, frequency of varicocele, smoking, alcohol ingestion, and body composition were considered. Statistical analysis was performed by SPSS program version 19.0 (SPSS Inc., Chicago, IL). Spearman correlation, Mann-Whitney test and regression model were applied. Statistical significance was considered with P value < 0. 05. The 25(OH)D average distribution concentration were significant lower in Abnormal seminal parameters group (P =0.016), and all parameters had a positive correlation with 25(OH)D serum levels. The highest coefficient value was observed in the association of total motility with Vitamin D (P =0.001). Our results demonstrated that 25(OH)D levels has a positive influence on spermatogenesis and semen quality, suggesting that vitamin D replacement should highly be concerned on male fertility treatment