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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental diabetes in animals induces marked alterations of gonadal androgenic functions: reduction in testis weight, morphological alterations of Leydig cells, decrease of plasma testosterone levels and reduction of the ability of the Leydig cells to secrete testosterone in vitro. hCG treatment restores the testicular endocrine function; in addition several morphological and functional changes are observed in the hypothalamic-hypophyseal-gonadal axis which are probably responsible for the testicular lesions found in untreated experimental diabetes mellitus. In diabetic men, the hypothalamic-hypophyseal-gonadal axis seems to be normal (with exception of individual cases); Mean plasma levels of testosterone, LH, FSH and the responses of the gonadal axis to hCG and LHRH are normal.
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PMID:[Hypophyseal-Leydig function in the diabetic]. 305 85

The regulation of testicular hCG binding and steroidogenesis in adult mutant mice with hereditary diabetes and obesity was studied. Low doses of hCG caused no change in hCG binding in obese (ob/ob) mice, whereas, in diabetic (db/db) mice, the increase in binding measured 24 h after hCG administration was not as great as in normal males. Intermediate doses of hCG caused a decrease in hCG binding in obese and normal mice, but not in diabetic animals. However, 72 h after injection of intermediate doses of hCG, a decrease in hCG binding also was observed in diabetic mice. Plasma testosterone was elevated 24 h after hCG injection in all types of mice studied, but the increase in diabetic mice was smaller than in normal animals. However, 72 h after treatment with hCG, plasma testosterone was still elevated in diabetic mice, but not in normal males. In vitro, hCG stimulated testicular testosterone synthesis in all groups of mice, but the observed increase was smaller in diabetic and obese than in normal animals. Plasma LH levels were higher in diabetic than in normal mice, whereas plasma FSH and prolactin levels were lower in obese mice than in normal animals. All parameters (i.e., LH receptors and circulating hormone levels) measured in yellow (Ay/a) mice were similar to those in normal (a/a) mice. The present study indicates that in these models for noninsulin-dependent diabetes, the testicular metabolism of LH receptors and capacity to secrete steroids is altered.
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PMID:Hormonal regulation of testicular human chorionic gonadotropin binding and steroidogenesis in adult mice with different forms of hereditary diabetes and obesity. 308 72

The National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK) provides the hFSH-I-3 preparation, to be employed as a tracer in the radioimmunoassay (RIA) of human follicle-stimulating hormone (hFSH). The contaminating LH contained in that preparation led us to study whether the iodination of such a material could render it a suitable tracer for RIA of both LH and FSH. hFSH-I-3 was labelled with 125I by the chloramine-T method and was further purified on Sephadex G-75 column. The LH-RIA was performed using this preparation and anti-LH at a final dilution of 1:37,500, with a sensitivity of 3 mIU LH/ml (2nd international reference pattern). The method was validated by comparing the LH values obtained in different serum samples with those obtained using the standard RIA (125I-LH/anti-LH); the correlation coefficient (r) was equal to 0.9988. No LH overestimation due to the putative cross-reaction with FSH was found. This was demonstrated by testing serum samples containing high (greater than 100 mIU/ml) and low (less than 10 mIU/ml) concentrations of FSH before and after the treatment with anti-LH. Under these conditions, serum samples from postmenopausal women, pregnant women, normal men and women in basal conditions and after the LH-RH administration, and from a patient with Klinefelter's syndrome, were evaluated. In conclusion, NIDDK 125I-hFSH-I-3 can be used as a tracer for the radioimmunological quantitation of both hLH and hFSH, which results not only inexpensive, but also allows to reduce the amount of the stored radioactive materials.
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PMID:Radioimmunoassays of human luteinizing and follicle-stimulating hormones using the same radioactive tracer. 311 67

In the present paper the following non-endocrine internal diseases are discussed: liver cirrhosis, diabetes, chronic renal failure and morbus Crohn. In alcoholic liver patients under fifty, hypospermia and oligozoospermia can be observed. The hormone assays showed moderately increased FSH- and LH-values in the serum; prolactin, testosterone and estradiol remained normal. An increased binding of testosterone to SHBG is supposed, and the androgen deficiency symptoms are considered to be due to the elevated binding of testosterone to SHBG. The other non-endocrine internal diseases and drug-groups (cytostatics, steroids, neuroleptics, antihypertensives, antiarrhythmics, nitrofurans, levamisole, fungicides and salazosulfapyridine) are reviewed on the basis of literature. After the administration of 1 g per day of cimetidine for four weeks in patients under fifty with duodenal ulcer, notable andrological side effects were not revealed by neither clinical nor hormone examinations.
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PMID:[Andrological abnormalities in internal diseases and following drug therapy]. 311 48

The clinical manifestations of primary or idiopathic hemochromatosis include mainly hepatomegaly, diabetes mellitus, and hypogonadism. Most investigators postulated that the hypogonadism is caused by pituitary dysfunction and that the deposition of iron in the testes is of little importance. We found not only pituitary failure in a 45-year-old man with idiopathic hemochromatosis (low LH and FSH levels, no response to GnRH) but could also detect by light microscopy deposition of iron in capillary endothelial cells and in the perivascular space of the testicular tissue. Electron microscopic study of tissue from the testes showed intracytoplasmic hemosiderin deposits in capillary endothelial cells. Abundant lipofuscin granules were present in Sertoli cells and Leydig cells. The serum testosterone levels were also lowered. In our opinion, the androgenic deficiency in idiopathic hemochromatosis is not only caused by pituitary failure but also by testicular dysfunction due to deposits of hemosiderin and lipofuscin in the testes.
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PMID:Idiopathic hemochromatosis in a 45-year-old infertile man. 312 99

In order to investigate the dopaminergic activity in diabetic women with secondary amenorrhoea we studied the response of prolactin to a dopamine receptor antagonist metoclopramide (MTC - 10 mg i.v.) in three groups of women: 5 insulin-dependent diabetic women with secondary amenorrhoea, 5 insulin-dependent diabetics with normal menstrual cycles and 6 non-diabetic women with regular cycles. Patients with diabetes and secondary amenorrhoea had significantly lower basal LH levels (P less than 0.001) and FSH levels (P less than 0.005) than normally cycling diabetic women. Basal and metoclopramide stimulated prolactin levels were lower in diabetic women with secondary amenorrhoea compared to normally cycling diabetics and control subjects. Evaluation of C-peptide levels in peripheral blood revealed that all amenorrheic diabetics had no endogenous beta cell function while diabetic women with normal cycles (except 1 patient) had preserved residual pancreatic beta cell secretion.
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PMID:Blunted prolactin response to metoclopramide in insulin-dependent diabetic patients with secondary amenorrhoea. 312 73

We have reviewed the role of insulin in ovarian physiology. Clinical observations and experimental data strongly support the hypothesis that insulin possesses gonadotropic activity, when acting alone or with FSH or LH. This idea is further supported by the recent discovery of insulin in follicular fluid. The idea that insulin has gonadotropic function can explain a variety of clinical observations, which otherwise are difficult to understand. For example, manifestations of ovarian hypofunction (primary amenorrhea, late menarche, anovulation, low pregnancy rate, and early menopause) in IDDM can be understood if it is accepted that insulin is necessary for the ovary to reach its full steroidogenic potential. The idea that insulin affects ovarian steroidogenesis also helps to understand the observation that hyperandrogenism frequently accompanies each of the various insulin-resistant states, regardless of the latter's etiology (e.g. genetic deficiency in the number of insulin receptors, antiinsulin receptor antibodies, obesity, etc.). The explanation for this association is based on the idea that hyperinsulinemia intensifies ovarian steroidogenesis, which manifests clinically as hyperandrogenism. Continuous stimulation of the ovary by insulin over a long period of time possibly produces morphological ovarian changes, such as hyperthecosis or polycystic changes; these changes commonly are observed among women with insulin resistance. The effects of insulin on ovarian cells are mediated possibly through binding of the peptide to its own receptor or to the IGF-1 receptor (the specificity spillover phenomenon). The latter could be an important mechanism in cases of insulin resistance. Potential mechanisms underlying the gonadotropic activity of insulin include direct effects on steroidogenic enzymes, modulation of FSH or LH receptor number, synergism with FSH or LH, or nonspecific enhancement of cell viability. The gonadotropic function of insulin adds yet another note to what has been termed a symphony of insulin action. Further investigation into this new area may yield greater insights not only into normal ovarian physiology, but also into the pathogeneses of such diverse entities as PCO, obesity, diabetes mellitus, and the syndromes of insulin resistance and acanthosis nigricans.
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PMID:The gonadotropic function of insulin. 330 17

Studies in the streptozotocin rat model for diabetes mellitus suggest that sexual dysfunction in these animals may result from diabetes-induced alterations of the neuroendocrine-reproductive tract axis. Our investigation was performed to better define the effects of diabetes on the neuroendocrine sex accessory organ axis in the male rat. Rats were rendered diabetic, and were either left untreated or treated with insulin, testosterone or both. Diabetes resulted in decreased body and reproductive organ weights, as well as diminished sperm counts and motility and prostatic acid phosphatase. Seminal fructose was increased. A significant decrease in serum LH, FSH and testosterone was noted. Insulin treatment of the diabetic rats restored serum gonadotropins, reproductive organ weight, sperm counts and motility, and seminal fructose to control levels. Prostatic weight and prostatic acid phosphatase levels remained abnormal. Testosterone restored the above mentioned parameters to control levels, with the exception of LH. Treatment with insulin and testosterone had a synergistic effect on spermatogenesis. A GnRH stimulation test demonstrated that pituitaries of diabetic animals had a blunted response, with diminished LH and FSH secretion. In the diabetic animal, there are both pituitary and testicular abnormalities which may be responsible for reproductive dysfunction.
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PMID:The effect of streptozotocin-induced diabetes on the neuroendocrine-male reproductive tract axis of the adult rat. 359 11

Plasma zinc and pituitary and testicular hormone concentrations were measured in two groups of male adolescents. One group comprised insulin-dependent diabetes mellitus patients, aged 14-19 years; the other, as control, included 12 healthy youngsters aged 13-19 years. Plasma concentration of zinc, prolactin, testosterone, and dihydrotestosterone were lower in diabetics than in controls, whereas the ratios of androstenedione and androstenedione to testosterone + dihydrotestosterone were higher. Plasma FSH and LH were normal. These results suggest a diminished conversion of androstenedione to testosterone and relate zinc with the 17-beta-hydroxysteroid dehydrogenase enzyme activity.
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PMID:Low plasma zinc and androgen in insulin-dependent diabetes mellitus. 374 Oct 26

The reduction of high serum LH levels toward or to normal in diabetic women in the menopausal range recorded during the first year of treatment with a synthetic progestin, 17-alpha-ethynyl-19-nortestosterone acetate, 3-cyclopentylenol ether (quingestanol acetate), was maintained during the second and third years of daily ingestion of this steroid. Normal LH and normal or high FSH levels prior to therapy were not affected. Other endocrine indices, including serum PBI and T4, plasma 11(OH) corticosteroids, serum growth hormone titers, insulin responses to oral glucose, and urinary excretion of 17-ketosteroids, Porter-Silber chromogens, and 11-desoxycortisol metabolites, estrogens, and creatinine remained relatively unchanged during quingestanol therapy. At the 36th month of treatment, a small increase in fasting blood glucose levels with greater hypoglycemia after oral carbohydrate was noted, but this probably reflected the natural history of treated diabetes mellitus. The decrease in urinary steroid responses to partial blockade of adrenal 11-beta hydroxylase by metyrapone observed in the 12th month of quingestanol therapy was not evident at the end of 24 and 36 months of treatment. Quingestanol therapy was associated with maintenance of the increase in serum sodium from low-normal to mid-normal concentrations noted during the first year of treatment. Serum chloride increases were less frequent. Other serum electrolytes, solutes, proteins and other nitrogenous constituents, lipids, and enzymes and formed blood elements generally fluctuated within the pre-therapy ranges. Body weight, blood pressure, pulse rate, electrocardiograms, and perception of vibrations were about the same prior to and at the completion of the three-year course of therapy. The steroid was well tolerated.
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PMID:Prolonged progestin (quingestanol) therapy of menopausal diabetic women. 446 59


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