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1.
J Androl ; 31(6): 584-92, 2010.
Article in English | MEDLINE | ID: mdl-20203339

ABSTRACT

To assess the effect of experimental Type 1 diabetes on male fertility, male Sprague Dawley rats were injected with either streptozotocine (STZ) to induce diabetes or with citrate buffer as controls. Diabetic animals and 2 control groups (STZ-resistant and buffer-injected rats) were sacrificed at 2 different times after injection: 6 weeks (6W) and 20 weeks (20W). We analyzed serum testosterone (sTT), epididymal sperm parameters, and weight of testicles and epididymides, and carried out a histological evaluation of testicular tissue. Diabetic animals presented a significant increase in teratozoospermia (20W, P < .01) and a decrease in sTT (P < .01), tubular diameter (6W, P < .05), and testicular (6W, P < .01) and epididymal (P < .01) weight. STZ-resistant animals showed significantly decreased sTT (6W, P < .01), epididymal weight (6W, P < .05), and sperm count (6W, P < .01) compared with buffer-injected controls. Experimental STZ diabetes increases teratozoospermia and decreases sTT, testicular weight (reverting at medium-term), and epididymal weight.


Subject(s)
Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Type 1/complications , Infertility, Male/etiology , Infertility, Male/physiopathology , Animals , Diabetes Mellitus, Experimental/pathology , Diabetes Mellitus, Type 1/pathology , Epididymis/pathology , Epididymis/physiopathology , Infertility, Male/pathology , Male , Organ Size , Rats , Rats, Sprague-Dawley , Semen Analysis , Testis/pathology , Testis/physiopathology , Testosterone/blood
2.
Int J Impot Res ; 16 Suppl 2: S10-2, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15496851

ABSTRACT

Prominent diseases of the endocrine system, such as diabetes mellitus, hypogonadism, and hyperprolactinemia, may cause erectile dysfunction (ED). ED affects about 50% of male diabetic patients possibly due to the vascular and neuropathic complications. Metabolic control and selective phosphodiesterase type 5 inhibitors are therapies of choice for controlling ED. By correcting hypogonadism, testosterone levels are restored. This, and the use of dopaminergic drugs, which normalize prolactin levels in male hyperprolactinemia, may be effective in reversing ED in these endocrine disorders.


Subject(s)
Diabetic Angiopathies/complications , Diabetic Neuropathies/complications , Erectile Dysfunction/etiology , Hyperprolactinemia/complications , Hypogonadism/complications , Diabetic Angiopathies/drug therapy , Diabetic Neuropathies/drug therapy , Erectile Dysfunction/drug therapy , Humans , Hyperprolactinemia/drug therapy , Hypogonadism/drug therapy , Male , Phosphodiesterase Inhibitors/therapeutic use , Testosterone/blood , Testosterone/therapeutic use
3.
Thyroid ; 11(8): 789-93, 2001 Aug.
Article in English | MEDLINE | ID: mdl-11525274

ABSTRACT

The cause of sporadic simple goiter is unknown in most cases. Family studies have suggested that this disorder may have a genetic component in some patients. We have previously demonstrated that some cases of endemic and nonendemic simple goiter are associated with a mutation within exon 10 of the thyroglobulin gene. Here we report a study of 50 cases diagnosed as having nonendemic simple goiter, and found 1 case with a large heterozygous deletion within the thyroglobulin gene. The deletion involves the promoter region and the 11 first exons of this gene and is associated with a euthyroid state. We hypothesize that the absence of thyroglobulin synthesis from the deleted allele may be responsible for a decreased level of thyroglobulin mRNA. Euthyroidism would be achieved by thyrotropin (TSH) stimulation but at the expense of goiter development.


Subject(s)
Gene Deletion , Goiter/genetics , Thyroglobulin/genetics , Aged , Alleles , Chromosome Mapping , Exons/genetics , Female , Heterozygote , Humans , Immunohistochemistry/methods , Polymerase Chain Reaction , Promoter Regions, Genetic/genetics , Reference Values , Staining and Labeling , Thyroid Gland/physiopathology
4.
Thyroid ; 6(5): 423-7, 1996 Oct.
Article in English | MEDLINE | ID: mdl-8936666

ABSTRACT

Iodine deficiency is the most relevant etiologic factor in endemic goiter. However, the fact that not all residents in the same area eventually develop goiter suggests that individual factors might also be involved in the etiology of endemic goiter. We have previously reported a point mutation in thyroglobulin exon 10 associated with nonendemic simple goiter. In an attempt to determine whether the mutation in thyroglobulin exon 10 might be linked to endemic goiter, we studied the genomic organization of thyroglobulin exon 10 in 36 patients diagnosed with endemic goiter by Southern blot, PCR, and sequencing analysis. We also analyzed by Southern blot the organization of the genomic region that contains thyroglobulin exons 1 to 11. In one case, we observed a point mutation in thyroglobulin exon 10. Sequencing analysis revealed a mutation at position 2610 of the cDNA, which implies a G to T substitution. This single base change results in a glutamine to histidine substitution and is the same as that previously reported by our group in patients with nonendemic goiter. To our knowledge, this is the first time that a mutation in the thyroglobulin gene has been described in a patient with endemic simple goiter and further confirms the association between the exon 10 mutation and development of goiter.


Subject(s)
Goiter, Endemic/genetics , Point Mutation , Thyroglobulin/genetics , Adult , Aged , Amino Acid Sequence , Base Sequence , Blotting, Southern , DNA Primers/genetics , DNA, Complementary/genetics , Exons , Female , Goiter, Endemic/etiology , Humans , Iodine/deficiency , Male , Middle Aged , Polymerase Chain Reaction , Restriction Mapping
5.
Rev Clin Esp ; 190(4): 191-4, 1992 Mar.
Article in Spanish | MEDLINE | ID: mdl-1589616

ABSTRACT

The case is presented of a young female with virilization signs and total circulating testosterone levels above 4 ng/ml, without a concomitant increase in cortisol, 17 OH-progesterone, DHEA-S, or androstenedion levels. On CT scan exam a tumoral mass in the left ovary was observed with polycystic characteristics similar to those observed in ovarian cystadenoma, inspite of the fact that most androgenic ovarian tumors are solid. The pathological study revealed an ovarian Sertoli-Leydig tumor associated to a reticular pattern with heterologous chondroid and mucinoid elements of cystadenoma.


Subject(s)
Leydig Cell Tumor/diagnosis , Ovarian Neoplasms/diagnosis , Sertoli Cell Tumor/diagnosis , Virilism/etiology , Adult , Cystadenoma/complications , Cystadenoma/diagnosis , Cystadenoma/pathology , Female , Hirsutism/diagnosis , Hirsutism/etiology , Hirsutism/pathology , Humans , Leydig Cell Tumor/complications , Leydig Cell Tumor/pathology , Leydig Cells/pathology , Male , Ovarian Neoplasms/complications , Ovarian Neoplasms/pathology , Ovary/pathology , Sertoli Cell Tumor/complications , Sertoli Cell Tumor/pathology , Sertoli Cells/pathology , Virilism/diagnosis , Virilism/pathology
6.
Arch Androl ; 25(1): 21-7, 1990.
Article in English | MEDLINE | ID: mdl-2389988

ABSTRACT

Spermatogenic function was studied in 10 patients, previously diagnosed as having primary hypothyroidism, in whom a state of hypothyroidism has been induced by discontinuation or a decrease in treatment with levothyroxine over at least one spermatogenic cycle. Most of the patients had fathered children before the study. When the results obtained in the hypothyroid state were compared with those from a group of 16 controls with proven fertility, slight anomalies were observed; these were characterized by a decrease in seminal volume (p less than 0.05), progressive forward motility (p less than 0.01), and the cumulative percentage of mobile forms (p less than 0.01). There were no anomalies in sperm density or in the percentage of spermatozoa with normal morphology. No alterations in circulating levels of testosterone and gonadotropins existed. Induction of hypothyroidism did not lead to seminal or hormonal modifications compared with the same patients in a situation of euthyroidism. Short-term postpuberal hypothyroidism did not cause seminal alterations sufficiently intense to induce male infertility.


Subject(s)
Hypothyroidism/physiopathology , Spermatogenesis , Humans , Hypothyroidism/blood , Hypothyroidism/chemically induced , Male , Substance Withdrawal Syndrome/complications , Thyrotropin/blood , Thyroxine/adverse effects , Thyroxine/blood , Triiodothyronine/blood
9.
Arch Androl ; 16(3): 247-51, 1986.
Article in English | MEDLINE | ID: mdl-2946270

ABSTRACT

Beta-endorphin (beta-ED) levels were evaluated in blood and seminal plasma of men with infertility due to varicocele, obstructive and nonobstructive azoospermia, and idiopathic oligoasthenospermia. The relation of this opiate to serum levels of gonadotropins, prolactin, testosterone, androstenedione, and dehydroepiandrosterone sulfate has also been investigated. beta-ED levels in seminal plasma were significantly higher than in blood plasma (p less than 0.001) in all persons studied. No statistically significant differences were found for beta-ED concentrations in semen or blood among any of the infertility situations studied. Nor were significant correlations observed between the concentration of this opiate and that of gonadotropins, prolactin, and androgens. The measurement of beta-ED in semen has little value in the differential diagnosis of male infertility. Nonetheless, its presence in high levels in semen must have some unknown function. Possibly, it comes from the various sites of the male reproductive tract, since no significant differences were found between obstructive and nonobstructive azoospermias.


Subject(s)
Endorphins/analysis , Infertility, Male/physiopathology , Androstenedione/blood , Dehydroepiandrosterone/blood , Endorphins/blood , Follicle Stimulating Hormone/blood , Humans , Luteinizing Hormone/blood , Male , Prolactin/blood , Semen/analysis , Testosterone/blood , beta-Endorphin
10.
Horm Metab Res ; 17(7): 366-9, 1985 Jul.
Article in English | MEDLINE | ID: mdl-4029878

ABSTRACT

The urinary kinetics of triiodothyronine (T3) in healthy young and old people has been studied. The behavior of urinary excretion is similar in both age groups, expressed in our mathematical model in the cumulative kinetics as well as in the urinary rate. However, a significant decrease (P less than 0.025) of renal clearance of T3 in elderly individuals has been found. No significant differences (P greater than 0.05) were observed in any other kinetic parameters. The possible influence of the reduction of glomerular filtrate has been discussed as the most important pathogenic factor of the decreased renal clearance of this hormone. Possibly, modifications of the distribution volumes are also involved. Due to the limited number of persons studied, for ethical reasons, the results obtained are not definitive.


Subject(s)
Aging , Triiodothyronine/urine , Adolescent , Adult , Aged , Glomerular Filtration Rate , Humans , Kidney/metabolism , Kinetics
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