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

A number of hormones and factors were found to stimulate growth of cultured rat islet tumor cells, the RIN-r cell line. A serum-free supplemented medium from RIN-r cells was formulated. It consisted of a 1:1 mixture of Ham's F12 and DME media with the addition of insulin, transferrin, triiodothyronine, prolactin, growth hormone, and an extract of proteose peptone (medium IM). The growth rate of RIN-r cells in this medium is as great as it is in 10% serum-supplemented medium. Up to 10 populations doublings occurred over a period of 20 days. Insulin is a very effective mitogen for RIN-r cells and has an effect on concentrations as low as 30 ng/ml. In addition, the insulin-like somatomedin, multiplication stimulating activity (MSA), is a growth factor at 50 ng/ml. It was found that RIN-r cells proliferate and continue to produce immunoreactive insulin in a hormonally and nutritionally defined medium. This medium is derived from medium IM, in which insulin is replaced with MSA and proteose peptone is omitted. Variations of this medium may prove useful in studies on the growth and function of the normal islets in long-term primary culture.
Diabetes 1981 Dec
PMID:Hormones and factors that stimulate growth of a rat islet tumor cell line in serum-free medium. 627 46

Subtotal tumour removal had been performed in a 34-year-old female patient for an extensive intra- and suprasellar expansive process. The considerably increased prolactin level did not decrease postoperatively, but normalised only after a three months bromocriptine treatment. The primary hyperthyroidism has been recovering after administering methimazolum. In a second case was reported on a 65-year-old female patient, suffering from rachitic dwarfism, stenosis of the aortic valve and tumour of the hypophysis, causing acromegaly, whose diabetes mellitus of contrainsular type could have been hardly balanced with insulin of a 128-unit-dose daily, and whose hyperthyroidism was due to an autonomous adenoma of the thyroid gland, first I-131 treatment was administered and she got into an euthyroid state. Six weeks following the removal of the acidophilic adenoma of the hypophysis administration of insulin could have been ceased, and the results of her growth hormone became normal. The clinical picture partly corresponds with Troell-Junet's syndrome.
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PMID:[Simultaneous occurrence of pituitary adenoma and thyrogenic hyperthyroidism]. 628 51

To determine the mechanism for the decrease of somatomedin levels in insulin-dependent diabetes, the relationships among plasma immunoreactive somatomedin-C (Sm-C), plasma growth hormone (GH) and prolactin (PRL), and the somatogenic and lactogenic binding sites in liver were assessed in rats with nonketotic diabetes mellitus of different duration (1 wk or 1 mo) and severity (50 or 60 mg streptozotocin/kg BW). One week after administration of 60 mg streptozotocin (STZ)/kg, plasma Sm-C concentrations were significantly decreased (0.23 +/- 0.03 versus 0.43 +/- 0.03 U/ml in controls; mean +/- SEM, P less than 0.01). In contrast, plasma GH concentrations, bovine GH (bGH) binding, and human GH (hGH) binding were not significantly changed. After 1 mo of diabetes, no further decrease in plasma Sm-C content was observed despite a reduction in plasma GH and PRL concentrations and reduced hepatic bGH binding capacity (5 +/- 2 versus 38 +/- 4 fmol/mg protein; P less than 0.01). In the group of rats injected with 50 mg STZ/kg, the Sm-C was reduced at 1 mo but hepatic GH binding was not. In a second study, diabetic rats (75 mg STZ/kg) were treated after 3 wk with insulin (10 U lente per day for 7 days). This treatment normalized Sm-C levels and partially restored the GH binding capacity (treated: 49 +/- 4 fmol/mg protein versus untreated diabetics: 28 +/- 6 fmol/mg protein; P less than 0.01 and versus controls: 68 +/- 4 fmol/mg protein; P less than 0.05).2+ suggest that in an early phase of nonketotic diabetes, the low plasma Sm-C is not due primarily to reduced GH receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 Nov
PMID:Low plasma somatomedin-C in streptozotocin-induced diabetes mellitus. Correlation with changes in somatogenic and lactogenic liver binding sites. 631 12

The effects of hypersecretion of growth hormone and prolactin on islet endocrine cells have been studied by radioimmunoassays, immunocytochemistry, and morphometry in randomized samples of pancreata from MtTW15 mammosomatotropic tumor-bearing and control rats. The randomized sampling procedure, validated by immunoassays, allowed evaluation of both hormone content (immunoassay) and endocrine cell population (immunocytochemistry) on samples derived from the same origin. Hyperinsulinemia (2x) and non-fasting hypoglycemia in 10-wk-tumor rats were normalized 3 wk after tumor removal. Pancreatic weight was doubled, but proportional to body weight increases. Islet/pancreas ratio was constant (1.29 +/- 0.05%) and the same in tumor, tumor-removed, and control animals, but average islet dimensions were increased by 30% and average area doubled in tumor animals. Frequency analysis showed fewer small (less than 70 micrometers) and more large (greater than 140 micrometers) islets in tumor animals, but no change in average islet shape shown by average axis ratios of 1.4 in all groups. Pancreatic content of insulin and glucagon was doubled, while that of somatostatin was constant. These changes were not completely reversed in tumor-removed animals. Similarly, a significant doubling in islet-derived mass was mainly due to a doubling of the B-cell mass as the average proportion of endocrine cells per islet shifted from 66%, 26%, and 18% to 81%, 18%, and 3% for B-, A-, and D-cells of control and tumor-bearing rats, respectively. Immunocytochemically detectable insulin was found in duct cells of tumor animals, but not controls. Whether such cells represent a functional reserve remains to be determined.
Diabetes 1983 Jan
PMID:Effect of MtTW15 mammosomatotropic tumors on pancreatic islet hormones. 633 5

We have evaluated the endocrine changes in 10 male subjects with hemochromatosis. Two subjects initially had aplastic anemia, and the remainder had idiopathic hemochromatosis. Four of the ten patients had diabetes mellitus. Sexual dysfunction (impotence and/or decreased libido) was observed in 8 subjects. Six patients had subnormal testosterone levels; FSH levels were almost uniformly low, but LH concentrations were more variable. Only three patients had normal testosterone responses to hCG. Hypothyroidism, free T4 less than 0.9 ng/dl, was present in 4 subjects, and the etiology was heterogeneous. Basal prolactin levels were elevated in 2 patients and failed to respond adequately to TRH in 2 other patients. Growth hormone reserve was normal in all but 1 patient, and pituitary-adrenal reserve was normal in all but 1 patient. We conclude that disturbances in both pituitary and end-organ function are observed in hemochromatosis. These central and end-organ defects may exist alone or simultaneously. Hypogonadism is almost universal, and is a consequence of defective function of the hypothalamic-pituitary axis and/or primary Leydig cell disturbance. Other evidence of pituitary disturbance are observed but are rather uncommon.
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PMID:The endocrine manifestations of hemochromatosis. 634 90

Animal experiments and clinical data indicate that prolactin (PRL) induces hyperinsulinemia and even diabetes. The effects of PRL on carbohydrate metabolism may be explained by at least two different mechanisms. Either PRL induces an insulin resistance at the peripheral tissue level, or PRL has a direct cytotropic effect on the pancreatic islets. Obviously, both mechanisms inducing hyperinsulinemia may coexist. We report here immunocytochemical evidence that PRL is localized in the endocrine pancreas of the normal adult rat. More precisely, the immunoreactive PRL is distributed in the cytoplasm of insulin-secreting B cells. These findings support a direct action of PRL on the endocrine pancreas.
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PMID:Immunocytochemical localization of prolactin-like immunoreactivity in rat pancreatic islets. 634 64

In normal and diabetic pregnancies, the placenta functions as a complex endocrine gland that modulates all classes of maternal nutrients to the fetus. The metabolic alterations of normal pregnancy are diabetogenic and associated with modest resistance to endogenous insulin. Pregnant women with carbohydrate intolerance represent three metabolically heterogeneous groups: type I (insulin-dependent), type II (non-insulin-dependent), and gestational diabetes. Patients with type I diabetes are at risk for ketosis and require replacement therapy because of a deficient production of insulin. They have decreased 24-hour, around-the-clock levels of C-peptide and glucagon, and lower nocturnal cortisol values and higher 24-hour prolactin levels than those of women with type II diabetes. Type II pregnant diabetic patients are not prone to ketosis and are more resistant to endogenous and exogenous insulin. They have higher fasting and meal-stimulated levels of C-peptide, accentuated fasting hypertriglyceridemia, and significantly lower high-density lipoprotein cholesterol levels than those of normal or type I women. In gestational diabetes, the metabolic stress of pregnancy evokes reversible hyperglycemia which may be associated with either a surfeit or a deficiency of insulin. These metabolic differences among diabetic pregnant women could have implications for placental structure and function that might influence fetal growth.
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PMID:Alterations of maternal metabolism in normal and diabetic pregnancies: differences in insulin-dependent, non-insulin-dependent, and gestational diabetes. 634 40

In the present studies, the content and the in vitro production of prolactin by decidua as well as the concentrations of prolactin in amniotic fluid, maternal and fetal serum in normal term pregnancies, induced abortions at various gestational ages, and in pregnancies complicated by diabetes mellitus, preeclampsia, chronic hypertension, and polyhydramnios were measured. Maternal and fetal prolactin levels varied considerably throughout gestation, but at term did not differ significantly between normal and abnormal pregnancies. Prolactin levels in amniotic fluid as well as decidual prolactin content and production were significantly lower only in pregnancies complicated by either hypertension or polyhydramnios. In both normal and abnormal pregnancies, decidual prolactin production correlated strongly with amniotic fluid concentrations. The present data suggest that 1) maternal and fetal prolactin levels do not differ significantly between normal and abnormal pregnancies, 2) the decidua is the principal source of amniotic fluid prolactin, and 3) the significantly lower levels of prolactin in amniotic fluid of pregnancies complicated by hypertension or polyhydramnios are probably due to adverse effects of these conditions on the synthesis and release of prolactin by decidua.
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PMID:Decidual, amniotic fluid, maternal and fetal prolactin in normal and abnormal pregnancies. 636 59

A sensitive and specific competitive enzyme-linked immunosorbent assay (ELISA) for rat prolactin was developed using reagents from the National Institute of Arthritis, Diabetes, Digestive Diseases and Kidney. In this assay soluble prolactin and prolactin adsorbed to a solid-phase support compete for rabbit anti-prolactin antibody binding sites. Therefore, a high concentration of soluble prolactin in the sample will result in a low concentration of antibody immobilized to the adsorbed prolactin. The immobilized antibody-prolactin complex is detected and quantified using goat anti-rabbit immunoglobulin G covalently conjugated to the enzyme horseradish peroxidase. Assay parameters were optimized by investigating the concentration of reagents and the reaction kinetics in each of the assay steps. The assay can be performed in 24 h. A sensitivity range of 0.06 to 6 ng in the region of 90 to 10% binding was obtained. Near 50% binding (0.6 ng), the intraassay coefficient of variation (CV) was 4.2% and the interassay CV was 7.6%. The correlation between radioimmunoassay and the ELISA was 0.868. Selected applications of the assay are described. The assay should prove a useful alternative to the radioimmunoassay in those instances where steps involving the use of 125I become limiting, for example, iodination facility and gamma counter availability or prolonged reagent storage.
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PMID:An enzyme-linked immunosorbent assay for rat prolactin. 637 40

The level of pituitary hormones (somatotropin and prolactin) and pancreatic hormones (insulin and glucagon) was measured by radioimmunoassay in blood of patients with insulin-independent diabetes mellitus with and without diabetic microangiopathies, in the state of decompensation and during treatment. Forty-four patients aged 26 to 60 years were examined. Some patients with insulin-independent diabetes with and without diabetic microangiopathies demonstrated an elevation of blood insulin and glucagon. The blood somatotropin level was found to be increased in patients with insulin-independent diabetes mellitus with diabetic microangiopathies in the state of decompensation. No correlations were established between prolactin and insulin levels, somatotropin and insulin levels in the blood of patients with insulin-independent diabetes mellitus. During treatment, one could see a decrease in the somatotropin content and a tendency toward elevation in the insulin content and reduction in the glucagon level in patients with insulin-independent diabetes with diabetic microangiopathies.
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PMID:[Levels of various pituitary and pancreatic hormones in the blood of patients with non-insulin-dependent diabetes mellitus]. 639 Apr 23


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