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

Thirty-six male patients with idiopathic haemochromatosis were subjected to measurements of basal plasma values of testosterone, LH and FSH and to an LRH test. Nineteen were also subjected to basal plasma determinations of T3, T4, cortisol, TSH and prolactin and to a TRH test. In 11 cases GH values were measured before, during and after an arginine infusion. Seventeen patients were found to hae low levels of testosterone, LH and FSH, and no gonadotrophin responses to LRH. Seventeen others had normal levels of these three hormones, with normal responses to LRH. The two remaining patients had normal testosterone values but very increased gonadotrophin values: a fact which remains unexplained. Basal levels of prolactin, GH, T3, T4, and TSH were normal: cortisol levels were either normal or increased in cases of poorly controlled diabetes. Prolactin responses to TRH were always normal. TSH responses to TRH were impaired in 2 cases, and GH responses to arginine in 3 cases. Considering that other factors may be involved in the few impairments found in TSH and GH stimulations, it is concluded that the only indisputable pituitary insufficiency in about half of the cases of idiopathic haemochromatosis is gonadotrophic.
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PMID:Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients. 679 82

The pituitary-testicular axis was investigated in the streptozotocin diabetic male rat to determine the relationship between hormonal alterations and steroidogenic activity. Male Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by intraperitoneal injection (40 mg/kg body wt.) of streptozotocin and they were studied with non-diabetic controls. The observations on these animals were compared to those from diabetic rats treated with 1-5 IU protamine zinc insulin. Steroidogenic activity was determined by measuring the per cent of [4-14C]-cholesterol converted to [4-14C]-pregnenolone and [4-14C]-progesterone. Plasma concentrations of LH, FSH and prolactin were measured by RIA. Streptozotocin induced diabetes resulted in significantly reduced plasma LH (34%, p less than 0.20) and prolactin (53%, p less than 0.001) but did not modify FSH concentrations. Insulin treatment completely and partially restored abnormal LH and prolactin release. The activity of the enzyme cleaving the side-chain of cholesterol (rate limiting step in steroidogenesis) was considerably reduced in the diabetic state (59%, p less than 0.002) and insulin treatment restored it to even supranormal levels (not significant). Our findings suggest that insulin may play a physiological and differential role in regulating the secretory activity of the anterior pituitary. The insulin is needed for normal LH and prolactin release and Leydig cells function but its role in FSH release and Sertoli cells function is not clear.
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PMID:Effect of streptozotocin diabetes on the pituitary-testicular axis in the rat. 681 42

Pituitary-gonadal function was studied in 50 male diabetic patients under 53 years of age. Forty-three had normal sexual activity and 7 were impotent. Plasma testosterone levels and urinary 17 ketosteroids, androsterone and dehydroepiandosterone levels were measured. LH and FSH levels before and after LHRH, and prolactin levels before and after TRH were also measured in plasma. No significant changes in pituitary-gonadal function were detected, irrespective of the patient's sexual activity. Neither the type and degree of control of diabetes nor the presence of absence of microangiopathy had any influence on the results. Basal LH and FSH levels were slightly higher in older patients. Prolactin levels after TRH were significantly higher in the later stages of the test in patients with microangiopathy.
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PMID:[Pituitary-gonadal function in male diabetic patients (author's transl)]. 707 53

A discussion of the side effects of hormonal oral contraceptive (OC) use is presented. Studies show that the estrogen component of OCs works to suppress the release of GRH (gonadotropin-releasing hormone), reducing the serum FSH level. The gestagen component desensitizes the frontal lobe of the pituitary gland to the effect of GRH and suppresses the preovulatory LH peak. OCs can cause subjective side effects such as nausea, headache, depression, which can also be observed during placebo use. Breakthrough bleeding, spotting, silent menstruation, and post-pill amenorrhea are menstrual irregularities which can be linked to OC use; 98% of those who discontinue OC use show normal biphasic menstrual cycles 3 cycles after discontinuation. A constant increase in serum triglyceride levels, small increases in cholesterol and phospholipid levels are observed among OC users. Minor cases of hyperinsulinism are observed among OC users with no history of diabetes; glucose tolerance tests should be regularly administered to OC users who have a risk of diabetes or a history of pregnancy diabetes. Serum levels of proteins are affected by OC use, probably due to the effects of OC use on liver function. Studies have shown an increased risk of thromboembolism and circulatory disorders among OC users, especially those who are over 30 years of age or who smoke. OC use has been linked to development of benign tumors of the liver and the cervix. Gestagens appear to reduce the frequency of endometrial mitosis. Other medications, e.g. analgesics, barbituates, can reduce the effectiveness of OCs. For adolescents, sequence preparations are preferred and should be administered only after a 1 year period of regular menstruation. Thorough check-ups should be performed on OC users twice yearly, and contraindications should be scrupulously observed.
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PMID:[Effects and side effects of hormonal contraceptives]. 741 48

A 47-year-old woman was evaluated for congenital dwarfism, primary amenorrhoea due to hypogonadotrophic hypogonadism, severe hyperlipidaemia with pancreatitis, and overt diabetes mellitus associated with severe insulin resistance requiring 2.5-3 units of insulin per kilogram body weight. Chromosomal analysis with trypsin banding was normal and biochemical evaluation revealed low oestrogen levels, inappropriately low gonadotrophins, very low IGF-I concentrations and GH concentrations unresponsive to insulin or L-dopa administration. Prolactin, pituitary-adrenal and pituitary-thyroid axes were normal. Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. A MRI of the brain revealed no discernible hypothalamic abnormalities and a small pituitary. The presence of congenital combined growth hormone and gonadotrophin deficiency on the basis of a suprapituitary defect suggests the existence of common or related pathways regulating GnRH and GHRH synthesis or secretion and may have contributed to the ultimate development of insulin resistance and hyperlipidaemia.
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PMID:Isolated combined growth hormone and gonadotrophin deficiency due to hypothalamic dysfunction, associated with insulin resistance. 755 20

Isolated porcine luteal cells from d 0-3 of the estrous cycle (estrus-d 0) were incubated with or without addition of 0, 10, 10(2) or 10(3) ng FSH/ml. Progesterone (P4) content was determined after 24 hrs of incubation. In nonstimulated conditions the basal P4 production of large cells (LCs) was 65 fold higher than that of small cells (SCs). The LCs but not SCs were stimulated by doses of 10 and 10(2) ng FSH. FSH in doses of 10 and 10(2) ng did not influence P4 production by SCs, but higher doses (10(3) ng) significantly decreased their P4 secretion The results indicated that FSH can have a distinct cellular luteotropic effect during the early development luteal phase of the pig. FSH influenced P4 secretion by LCs whereas, with SCs it had no effect (10 and 10(2) ng) or P4 secretion decreased (10(3) ng).
Exp Clin Endocrinol Diabetes 1995
PMID:Effect of FSH on progesterone secretion by porcine large and small luteal cells isolated from early-developing corpora lutea. 758 35

The aim of the present study was to evaluate the effect of low dose GnRH analogue (Buserelin) on gonadal steroid secretion and hair growth in hirsute women. The drug was administered as a nasal spray (200 micrograms tid) to reduce gonadal steroid secretion. Eight hirsute women were treated for six month with the gonadotropin-releasing hormone analog. All had subclinical polycystic ovary syndromes on the basis of ultrasound or hormonal data, together with ovary dysfunctions and irregular menses. None had adrenal or pituitary dysfunction. The score of hirsutism was evaluated according to Ferriman and Gallway; pituitary function was evaluated measuring the FSH and LH response to GnRH stimulation and gonadal steroid secretion by measuring estradiol, progesterone, total plasma testosterone, androstenedione and androstanediol. Sex hormone binding globulin, insulin, prolactin and DHEA-S were also measured. The suppression of ovarian steroid secretion was confirmed by reductions in total plasma testosterone, and rostenedione and androstanediol that were detectable after one month of treatment. FSH and LH responses to GnRH stimulation were inhibited consistent with pituitary desensitization. No significant side effects were observed and all patients completed the trial. The score of hirsutism was 24 +/- 5 before, 19.6 +/- 6 by the 3rd month and 16.8 +/- 5.1 by the 6th month of treatment (p < 0.001); the effect was still evident 1 and 6 months after the withdrawal of the therapy (14.8 +/- and 15.8 +/- 5 respectively; p < 0.001). Our findings indicate that Buserelin is useful in the treatment of non adrenal hirsutism when other forms of therapy are contraindicated or poorly tolerated by the patient.
Exp Clin Endocrinol Diabetes 1995
PMID:Efficacy of low-dose GnRH analogue (Buserelin) in the treatment of hirsutism. 762 Oct 99

The present study investigated the impact of high estrogen doses on melatonin blood concentrations in healthy young girls. Melatonin secretion was investigated in 7 girls (chronological age 13.2 +/- 0.2 years; bone age 12.8 +/- 0.2 years) before and during treatment with ethinylestradiol (EE2, daily dose 0.5 mg/d orally) aimed at the reduction of final prospective height in familial tall stature. Melatonin, LH, FSH, E2 and EE2 were measured by radioimmunoassay. In all subjects, LH and FSH were completely suppressed, but melatonin secretion, day/night plasma values as well as the area under the curve (AUC) remained unchanged under pharmacological administration of ethinylestradiol. We therefore conclude that melatonin secretion is not affected by pharmacological doses of the synthetic estrogen derivative ethinylestradiol in healthy young girls. The decrease of melatonin blood concentrations during puberty is not caused by increasing concentrations of estrogens but must be due to some other process.
Exp Clin Endocrinol Diabetes 1995
PMID:No effect of ethinylestradiol treatment on melatonin secretion in healthy pubertal girls. 762 Nov 5

Patients referring to the Urology and/or Endocrinology Departments of Ankara Medical School with complaints of diabetes mellitus (DM) and related complications were evaluated during the last year. A detailed history was obtained and all of the patients were questioned especially about sexual function problems. Following this evaluation, all patients were divided into two main groups, i.e. patients with sexual disorders, and those with normal sexual function. Factors such as BPH, cerebrosclerosis and other important vascular-neurologic pathologies which may play a role in the etiology of impotence were excluded from the study and 38 patients with sexual dysfunction and 15 with normal sexual activities have undergone further evaluation. Following routine blood and urine analyses, serum hormone levels (testosterone, FSH, LH, prolactin) were determined. Penile color-flow doppler analysis, cavernosometry, cavernosography, bulbocavernous reflex latency time and evaluation of somatosensory evoked potentials were performed. Additionally, all patients were evaluated from the psychiatric aspect using the Hamilton depression scale and MMPI questionnaire. The presence of vascular or neurologic pathology in 89.4% of our patients and of both pathologies in 39.4% of the patients, indicated the importance of multifactorial evaluation of diabetic impotence in order to plan a complete and efficient therapy program.
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PMID:Multidisciplinary evaluation of diabetic impotence. 771 29

In polycystic ovarian disease there is a strong association between hyperinsulinemia and hyperandrogenism but not with obesity alone. The magnitude of peripheral insulin resistance is similar to that seen in non-insulin-dependent diabetes mellitus. Mild hyperinsulinemia in PCOD patients is not impair the carbohydrate metabolism. The elimination of the cause of hyperandrogenism by bilateral oophorectomy, long-acting Gn-RH agonist or antiandrogen cyproterone acetate did not improve the associated insulin resistance. In opposition to insulin resistance in the tissues responsible for metabolism of carbohydrate, the ovary remains sensitive to the effects of pancreatic hormone. Presumably this mechanism involved the interaction with IGF-I receptors to stimulate thecal and stromal androgen production. Insulin may sensitize the stroma to the stimulatory effect of LH. In the mechanism of follicular arrest take part increased level of binding proteins for IGF-I, mainly IGFBP 2, -4 and 5 inhibit FSH and IGF-I action.
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PMID:[Insulin resistance in the pathogenesis of polycystic ovarian disease (PCOD)]. 772 20


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