Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothalamic regulatory hormones used for clinical studies are TRH, Gn-RH and somatostatin. In addition, as dopamine appears to be a physiological PIF, the dopamine agonists such as bromocriptine, could be considered as functional analogues of PIF. Gn-RH can be used to study the hypothalamic-pituitary gonadal relationship and to test the secretory reserve capacity of the gonadotrophs in disease states. Unfortunately Gn-RH testing discrimulates between pituitary and hypothalamic diseases only poorly. However gonadotrophin deficient men or women may be successfully treated with long-term Gn-RH with induction of puberty, potency, spermatogenesis and ovulation. Somatostatin has multiple actions in inhibiting endocrine and exocrine secretion but its actions are still being explored in diabetes. Bromocriptine, a long acting dopamine agonist (a functional analogue of PIF), suppresses prolactin and is highly effective in treating many hypogonadal states since hyperprolactinaemia is common. It also lowers growth hormone in acromegaly. TRH has provided a major, accurate, sensitive and safe test of thyroid function.
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PMID:Hypothalamic regulatory hormones: physiological and clinical implications. 2 68

Blood prolactin levels were measured under basal conditions and following the intravenous injection of TRH at time 0, 30, 60 and 120 minutes in 22 men and 21 women insulin-dependent diabetics, aged less than 50 years and not taking any drug influencing prolactin secretion. Prolactin levels were significantly higher (alpha = 0.05) at the 120th minute in male diabetics and under basal conditions and at the 60th minute in female controls. There was no correlation with retinopathy, age and control of diabetes. At the 30th minute, prolactin levels were higher when diabetes was of more recent onset. These results confirm the absence of any participation of prolactin in the development of retinopathy, although variations in prolactin may be seen in association with the presence of diabetes.
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PMID:[Blood prolactin in insulin-dependent diabetics. Basal study and effect of stimulation]. 9 21

The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.
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PMID:Prolactin response to TRH in diabetic ketoacidosis. 11 89

Prolactin levels were measured in 84 patients aged 20 years with hypogonadism, both under baseline conditions and after stimulation with TRH. In those with impuberty from delayed puberty or gonadotropin insufficiency, baseline blood prolactin levels were normal but the response after stimulation was reduced in a significant manner. In patients with Klinefelter's syndrome, both baseline and reserve blood prolactin levels were increased. No correlation was observed between these abnormal levels and the usual clinical and biological disturbances found in this disorder (gynaecomastia, diabetes, hyperinsulinism, changes in 5-alpha-reduction). The significance of this hyperprolactinaemia remains obscure.
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PMID:[Blood prolactin levels in male hypogonadism (author's transl)]. 12 17

The estrogen-binding capacity of mammary tumors induced by 7,12-dimethylbenz(a)anthracene was measured in lesions from animals after the ovariectomy, deprival of insulin (diabetes), or treatment with lergotrile mesylate to inhibit prolactin secretion. The average estrogen-binding capacity was 30 fmoles/mg cytosol protein in growing or static carcinomas from intact (control) animals. A significant reduction in estrogen-binding capacity was observed in regressing but not static mammary tumors from ovariectomized animals. In regressing and static tumors from diabetic rats, estrogen-binding capacity was significantly lower than in lesions from intact animals; this effect was not seen in growing tumors from diabetic rats. Tumors that were growing or static in lergotrile-treated animals showed reduced capacity to bind labeled estradiol. The effects of duration of hormone treatment or time of tissue storage on estrogen-binding capacity were examined and did not appear to be correlated with the decreased binding in tumors from treated animals. The results suggest that hormones capable of producing altered neoplastic growth may influence the level of estrogen receptors.
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PMID:Influence of hormonal alteration of host on estrogen-binding capacity in 7,12-dimethylbenz(a)anthracene-induced mammary tumors. 13 55

Ultrastrucutral examination of 184 pituitary adenomas demonstrated the presence of extracellular accumulations of electron dense material in 3 out of 64 cases with acromegaly. Fibrillary structures were seen in larger deposits of such material. This material was only observed in biopsies fixed directly with osmium tetroxide; initial fixation with glutaraldehyde did not retain the material and left empty spaces. Positive immuno-histochemical reaction with specific antibodies demonstrated that the extracellular material contained growth hormone (GH). The presence of this extracellular material could not be related to the age or sex of the patient nor to the duration of symptoms, size of the tumor, presence of diabetes mellitus, or concomitant secretion of prolactin. The pericapillary fibrous sheath was heavily thickened in the patient with the longest duration of symptoms, intermediate in thickness in the second and normal in the third.
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PMID:Extracellular growth hormone deposits in pituitary adenoma. 14 77

Alteration of growth of dimethylbenz[a]anthracene-induced mammary tumors was caused by removal of estrogen (ovariectomy), or insulin (diabetes), or by inhibition of prolactin secretin (treatment with an ergoline derivative). The levels of cyclic AMP (cAMP) and cGMP were measured in carcinomas classified as growing, static, and regressing. The amount of cAMP, expressed as pmoles/mg tumor weight or pmoles/mg protein, was lowest in growing tumors, intermediate in static tumors, and highest in those regressing. No correlation was seen between tumor growth and cGMP levels. Cyclophosphamide-induced tumor stasis did not elevate cAMP levels. The data suggest a role of cAMP in arrest of hormone-induced tumor growth.
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PMID:Relationship of adenosine 3',5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate to growth of dimethylbenz(a)anthracene-induced mammary tumors in rats. 17 3

Specific iodine-125-labeled prolactin binding was measured in membrane particles prepared from R3230AC mammary carcinoma and liver of tumor-bearing Fischer rats after either prolactin, estrogen, or lergotrile mesylate treatment, or after the induction of diabetes by streptozotocin. Hormone binding to tumors was decreased by treatment with prolactin (.5 or 1 mg/day) or estradiol valerate (7.5 mg/kg/week). In contrast, prolactin treatment was without affect on prolactin binding to liver membrane particles, but estradiol valerate treatment resulted in a 4-fold increase in prolactin binding to this tissue. Lergotrile mesylate, which lowers plasma prolactin levels, had no affect on tumor growth or prolactin binding to either tumor or liver. Prolactin binding to both tumor and liver was significantly reduced in diabetic rats, suggesting that insulin may play an important role in controlling tissue sensitivity to prolactin. Specific binding of iodine-labeled prolactin to enzymatically dissociated cells from R3230AC tumors was demonstrated in vitro. The binding capacity of the cells was found to be of the same order of magnitude as the binding capacity in membrane preparations when appropriate corrections were applied for yields of cells and membranes. R3230AC tumor, which is responsive to prolactin, appears therefore to be a useful model system for further study aimed at elucidation of growth and metabolic response to the hormone prolactin in breast cancer.
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PMID:Prolactin binding to R3230AC mammary carcinoma and liver in hormone-treated and diabetic rats. 18 51

The prevalence of sexual dysfunction and the pituitary-gonadal function were studied in 72 consecutive diabetic male patients. Sexual dysfunction was found in 43% and in these patients peripheral neuropathy was significantly more frequent than in patients with normal sexual function. Sexual dysfunction was more frequent in patients at the age of 50--55 years than in young diabetics (age 25--30 years). No significant correlation between sexual dysfunction and the duration of the disease and no difference in the serum concentrations of luteinizing hormone, follicle stimulating hormone, prolactin, testosterone and oestradiol-17beta between patients with normal and reduced sexual function was found. It is concluded, that sexual dysfunction is not accompanied by altered serum concentrations of testosterone, oestradiol 17beta, gonadotrophins or prolactin. Sexual dysfunction correlates with peripheral neuropathy, but the high prevalence of dysfunction in males with short duration of diabetes without neuropathy makes other causes likely.
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PMID:Sexual function and pituitary axis in insulin treated diabetic men. 28 15

Five men and three women with active acromegaly were treated with bromocriptine. After three months' therapy (30 mg/day) mean GH during the day decreased by 50% in six out of eight subjects. In the remaining two subjects (non-responders) GH was persistently over 100 micrograms/l. Mean GH during glucose tolerance test were not significantly decreased in three out of the eight subjects, of whom two were the nonresponders. The minimum dose of bromocriptine required to achieve maximum GH suppression ranged from 7.5 to 20 mg/day. In contrast, serum prolactin (PRL) throughout the day suppressed significantly in all subjects after 5 mg/day bromocriptine. Decreases in clinical symptoms, hand volume, urinary hydroxyproline and calcium excretion were seen in about half of the subjects. Three of the four subjects with diabetes mellitus showed improvement in glucose tolerance. Although minor side effects were uncommon, one patient died because of massive gastrointestinal haemorrhage from a duodenal ulcer.
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PMID:Treatment of acromegaly with bromocriptine. 28 87


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