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

Some data in the literature suggest that heightened activity of the pineal gland may be diabetogenic. The onset of insulin-dependent diabetes mellitus is highest during the winter months and at puberty when melatonin levels are also greatest. To study the direct effects of pineal hormones on insulin release, hand-dissected ob/ob-mouse islets of Langerhans were incubated in vitro with melatonin (1 nmol/l to 100 mumol/l) or arginine vasotocin (1 pmol/l to 10 mumol/l) and D-glucose (3 or 20 mmol/l for 1 hr. Melatonin did not affect basal or glucose-stimulated insulin release. Arginine vasotocin (AVT) did not affect basal insulin release, but at presumably pharmacological levels (1 and 10 mumol/l) the peptide significantly increased glucose-stimulated insulin release. We conclude that melatonin and AVT at physiological concentrations have no direct effect on islet insulin release, and that any diabetogenic effect of the pineal gland must occur via suppression of insulin action or via production of a metabolite or hormone that suppresses insulin release.
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PMID:Insulin release from isolated mouse islets in vitro: no effect of physiological levels of melatonin or arginine vasotocin. 179 24

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

Melatonin (in gum tragacanth as solvent) was administered to mice in the dose range of 100 to 450 mg/kg intraperitoneally. It prevented the increase in plasma glucose resulting from pancreatic toxicity caused by the intravenous administration of alloxan at 40 mg/kg. This action of melatonin was significant and dose-dependent. In parallel work using mouse brain homogenates, melatonin and more so its principal hepatic metabolite, 6-hydroxymelatonin, inhibited the formation of colored products reacting with thiobarbituric acid. Again, this inhibition was significant and dose-dependent. Alloxan-induced diabetes and lipoperoxidation induced by thiobarbituric acid are imputed to the production of oxygen free radicals. The consistent results obtained using these two experimental models show the antioxidant activity of melatonin, both in vivo and in vitro. This effect may be reasonably attributed to the indole structure of the molecule.
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PMID:Antioxidant activity of melatonin in mice. 832 21

Alterations in periodical functions are known to occur in aging and may be regarded as markers of the aging process itself. Melatonin and Thyroid Stimulating Hormone (TSH) circadian periodicities were studied in 22 aged subjects and in 13 adult controls. The study of rhythmicity was performed by the Cosinor analysis. Elderly subjects were hospitalized because of various concomitant diseases. Circadian periodicity of both hormones was disrupted in the aged group, and the deterioration of melatonin periodicity was significantly correlated with the decay in cognitive functions, quantified by the Mini Mental State evaluation. Diabetes was also found to affect, though not significantly, melatonin, but not TSH, periodicity. Melatonin and TSH nocturnal peaks were decreased in aged people. TSH oscillation amplitudes were inversely correlated with age. No correlation was found between melatonin and TSH secretory features both in adult and in aged subjects.
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PMID:Circadian secretion of melatonin and thyrotropin in hospitalized aged patients. 848 24

Currently available as a dietary supplement, the pineal hormone melatonin is portrayed by the media as a formidable weapon against disease and aging. Accordingly, primary health care providers should be cognizant of which of its proposed uses are supported by biomedical research and which are, as yet, unproven. Melatonin entrains circadian rhythms and, thus, can treat jet lag, delayed sleep phase syndrome, and sleep disorders in the blind and in some neurologically impaired children. By virtue of its hypnotic effect, melatonin can mitigate insomnia in the elderly. Reductions in melatonin secretion have been associated with many disorders, including cardiovascular disease, Alzheimer's, diabetes, SIDS, and aging; however, melatonin's role in their etiology and/or pathophysiology is unproven. Preliminary studies suggest a possible adjuvant therapeutic role for melatonin in cancer therapy. Melatonin secretion is reduced by alcohol, caffeine, and some commonly prescribed drugs. Since tolerance, fatigue, and other side effects have been reported, melatonin use on consecutive nights should be avoided and only the lowest effective hypnotic dose should be taken.
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PMID:Melatonin: media hype or therapeutic breakthrough? 905 17

The direct influence of indoleamines on ovarian peptide hormones and growth factor secretion, in contrast to steroidogenesis, is yet to be thoroughly investigated. The aim of our in vitro experiments was to investigate the influence of melatonin and serotonin (5-hydroxy-tryptamine) (0.01-10 micrograms/ml) on the release of insulin-like growth factor-I (IGF-I), oxytocin and progesterone by cultured human granulosa cells. It was observed that both melatonin and serotonin stimulate IGF-I release. Melatonin also stimulated oxytocin output. Serotonin increased oxytocin secretion only at the highest dose (10 micrograms/ml). Both melatonin and serotonin were potent inhibitors of progesterone release. The present results suggest a possible involvement of the indoleamines melatonin and serotonin in the direct regulation of growth factor, nonapeptide and steroid hormone secretion by human ovarian cells.
Exp Clin Endocrinol Diabetes 1997
PMID:Melatonin and serotonin regulate the release of insulin-like growth factor-I, oxytocin and progesterone by cultured human granulosa cells. 913 42

We have studied the effect of the administration of two doses of melatonin (melatonin 100 and melatonin 200 microg/kg bw) on diabetes and oxidative stress experimentally induced by the injection of streptozotocin (STZ) in female Wistar rats. STZ was injected as a single dose (60 mg/kg i.p. in buffered citrate solution, pH 4.0) and melatonin (melatonin 100, 100 microg/kg/day i.p.; melatonin 200, 200 microg/kg/day i.p.) beginning 3 days before diabetes induction and continuing until the end of the study (8 weeks). The parameters analysed to evaluate oxidative stress and the diabetic state were a) for oxidative stress, changes of lipoperoxides (i.e., malondialdehyde, MDA) in plasma and erythrocytes and the changes in reduced glutathione (GSH) in erythrocytes and b) for diabetes, changes in glycemia, lipids (triglycerides: TG; total cholesterol: TC; HDL-cholesterol, HDL-c), percentage of glycosylated hemoglobin (Hb%), and plasma fructosamine. The injection of STZ caused significant increases in the levels of glycemia, percentage of glycosylated hemoglobin, fructosamine, cholesterol, triglycerides, and lipoperoxides in plasma and erythrocytes, whereas it decreased the levels of HDL-c and the GSH content in erythrocytes. The melatonin 100 dose reduced significantly all these increases, except the percentage of glycosylated hemoglobin. With regard to the decreases of plasma HDL-c and GSH content in erythrocytes, this melatonin dose returned them to normal levels. The melatonin 200 dose produced similar changes, though the effects were especially noticeable in the decrease of glycemia (55% vs. diabetes), percentage of hemoglobin (P < 0.001 vs diabetes), and fructosamine (31% vs. diabetes). This dose also reversed the decreases of HDL-c and GSH in erythrocytes. Both doses of melatonin caused significant reduction of the percentage of glycosylated hemoglobin in those groups that were non-diabetic. These illustrate the protective effect of melatonin against oxidative stress and the severity of diabetes induced by STZ. In particular, this study confirms two facts: 1) the powerful antioxidant action of this pineal indole and 2) the importance of the severity of oxidative stress to maintain hyperglycemia and protein glycosylation, two pathogenetic cornerstones indicative of diabetic complications. Melatonin reduces remarkably the degree of lipoperoxidation, hyperglycemia, and protein glycosylation, which gives hope to a promising perspective of this product, together with other biological antioxidants, in the treatment of diabetic complications where oxidative stress, either in a high or in a low degree, is present.
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PMID:Oxidative stress in diabetic rats induced by streptozotocin: protective effects of melatonin. 975 30

Human and rat pineal melatonin secretion decline with aging, whereas visceral fat and plasma insulin levels increase. Melatonin modulates fat metabolism in some mammalian species, so these aging-associated melatonin, fat and insulin changes could be functionally related. Accordingly, we investigated the effects of daily melatonin supplementation to male Sprague-Dawley rats, starting at middle age (10 months) and continuing into old age (22 months). Melatonin was added to the drinking water (92% of which was consumed at night) at a dosage (4 microg/ml) previously reported to attenuate the aging-associated decrease in survival rate in male rats, as well as at a 10-fold lower dosage. The higher dosage produced nocturnal plasma melatonin levels in middle-aged rats which were 15-fold higher than in young (4 months) rats; nocturnal plasma melatonin levels in middle-aged rats receiving the lower dosage were not significantly different from young or middle-aged controls. Relative (% of body wt) retroperitoneal and epididymal fat, as well as plasma insulin and leptin levels, were all significantly increased at middle age when compared to young rats. All were restored within 10 weeks to youthful (4 month) levels in response to both dosages of melatonin. Continued treatment until old age maintained suppression of visceral (retroperitoneal + epididymal) fat levels. Plasma corticosterone and total thyroxine (T4) levels were not significantly altered by aging or melatonin treatment. Plasma testosterone, insulin-like growth factor I (IGF-I) and total triiodothyronine (T3) decreased by middle age; these aging-associated decreases were not significantly altered by melatonin treatment. Thus, visceral fat, insulin and leptin responses to melatonin administration may be independent of marked changes in gonadal, thyroid, adrenal or somatotropin regulation. Since increased visceral fat is associated with increased insulin resistance, diabetes, and cardiovascular disease, these results suggest that appropriate melatonin supplementation may potentially provide prophylaxis or therapy for some prominent pathologies associated with aging.
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PMID:Daily melatonin administration at middle age suppresses male rat visceral fat, plasma leptin, and plasma insulin to youthful levels. 992 36

Many environmental and occupational agents have been shown to cause detrimental effects on endocrine function and growing scientific evidence supports the hypothesis that such alterations may produce serious consequences for health. Although those chemicals mimicking (or contrasting) estrogenic or androgenic actions have raised great concern, the relevance of disruption of other hormonal pathways is not negligible. This article reviews the effects of chemical and physical agents on the hypothalamus-pituitary unit, pineal gland, thyroid, parathyroid and calcium metabolism, adrenal glands, and glucose metabolism. Metals (Pb, Mn, Cd, organotin compounds), solvents (benzene, dioxane, styrene, tetrachloroethylene, toluene), organochlorines (PCBs, TCDD), and physical agents have been shown in human, animal or in vitro studies to cause alterations of the blood levels, and of the activity or circadian rhythm of pituitary hormones. Melatonin has been proposed as the link between environmental/occupational factors and the immunologic and neoplastic diseases, which in addition to disturbances of the circadian timing system, feature pineal hormone reduction. Thyroid gland diseases (goiter, autoimmune thyroiditis, carcinoma) are associated with exposure to many chemical or physical agents. Disruptions of calcium control secondary to metal exposures, as well as the effect of radiation on parathyroid, are addressed. Adrenal cortex and medulla function alterations by several chemical agents are considered. Finally, diabetes mellitus as an outcome of occupational or environmental exposures and as susceptibility to occupational and environmental factors is discussed.
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PMID:[Occupational agents and endocrine function: an update of the experimental and human evidence]. 1059 41

Increased melatonin secretion observed in male patients with congenital isolated hypogonadotropic hypogonadism and its normalization during testosterone treatment had suggested that melatonin and the reproductive hormones are inter-related. Since these patients have a congenital form of hypogonadism, it is likely that hypermelatoninemia is the consequence of hypogonadism. To further study the relations between the pineal and the reproductive axis in humans, we evaluated melatonin secretion in two men (aged 35 and 50 yrs.) with acquired adult-onset hypogonadotropic hypogonadism. The diagnosis was based on the findings of normal testicular volume, azoospermia, low serum testosterone, normal LH and FSH levels, but apulsatile LH secretion, and intact anterior pituitary hormones secretion, normal findings on skull radiographic imaging, prior sexual maturation and paternity. Melatonin secretion was assessed as urinary 24 h 6-sulphatoxymelatonin excretion (aMT6s) prior to and during the administration of 250 mg testosterone enanthate per month for 4 months. Pretreatment melatonin production was markedly increased in both patients: 427-915 ng/kg/24 h vs. 204+/-81 [mean+/-SD] in 16 age-matched male controls. During testosterone treatment, aMT6s levels were normalized in one patient (range: 81-287 ng/kg/24 h) and remained elevated in the other patient (range: 830-1280 ng/kg/24 h). These data indicate that male patients with acquired GnRH deficiency have increased melatonin secretion. Melatonin hypersecretion in these patients may reflect a functional association.
Exp Clin Endocrinol Diabetes 2000
PMID:Melatonin hypersecretion in male patients with adult-onset idiopathic hypogonadotropic hypogonadism. 1082 23


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