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

It is well established that specific binding sites for insulin are present on the plasma membranes of target tissues. In order to explain how insulin regulates a wide variety of biologic functions both on the surface of the cell as well as in its interior, it has been postulated that insulin generates a second messenger at the cell surface. To date, however, no second messenger for insulin has been identified that can carry out all of insulin's known actions. Recent studies have demonstrated that, in addition to the plasma membrane, other subcellular organelles, such as the nucleus, have specific binding sites for insulin. There is also evidence indicating that large serum proteins such as albumin, large protein hormones such as prolactin, and small protein hormones such as insulin can enter intact cells. It is hypothesized, therefore, that insulin has at least two mechanisms of action on target tissues. One mechanism entails the direct binding of insulin to the plasma membrane, which in turn leads to its well-known effects on membrane transport. The other mechanism requires the entry of insulin itself into the interior of the cell and its subsequent direct binding to subcellular organelles. This latter process then serves to mediate many of the known intracellular functions of insulin.
Diabetes 1977 Feb
PMID:Does insulin need a second messenger? 32 74

A family had three siblings affected with classic Friedreich's ataxia. One sibling died at age 20 with fulminant diabetic ketoacidosis. The other two affected siblings are identical twin sisters without clinical diabetes but with an abnormality in the metabolism of exogenously administered glucose. These twins also have abnormal hypothalamic-pituitary control of prolactin and possibly of growth-hormone secretion. This study extends the previous reports of endocrine deficienceis associated with Friedreich's ataxia. The mechanisms underlying this association are undetermined but could represent pleiotropic effects of the Friedreich's ataxia gene or secondary manifestations of the primary central nervous system degeneration, or both.
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PMID:Abnormal function of endocrine pancreas and anterior pituitary in Friedreich's ataxia. Studies in a family. 34 4

Growth rates of 7,12-dimethylbenz(a)anthracene-induced mammary tumors and the specific 125I-labeled prolactin binding to membrane fractions prepared from livers and tumors were studied in rats made diabetic by streptozotocin injection. Growth was inhibited in a majority of tumors and prolactin binding was reduced in both tumors and livers from diabetic animals. Prolactin binding to individual tumors varied over a wide range in both intact and diabetic animals. Scatchard analysis of binding data revealed that the apparent affinity of prolactin binding to liver and tumor membranes was similar (Ka approximately 3.0 X 10(9) M-1) and was not affected by diabetes. We suggest that the reduction in prolactin binding to tumors may render these tissues less responsive to prolactin and thereby explain, at least in part, the observed inhibition of tumor growth in diabetic rats. However, some tumors in diabetic animals regressed despite relatively high levels of prolactin binding activity. Therefore, additional factors most certainly play important roles in the mechanism(s) by which the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is impaired in the diabetic rat.
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PMID:Prolactin binding to 7,12-dimethylbenz(a)anthracene-induced mammary tumors and liver in diabetic rats. 40 90

118 sterile men and 12 normal control patients, aged 20-38, were tested to determine the effect of luteinizing hormone-releasing hormone (LH-RH) on the gonadotropin levels and thyroid releasing hormone (TRH) on the prolactin level. The 118 sterile men were classified as suffering either from moderate oligospermia or excretory zoospermia (Group 1) or severe secretory oligo- or azoospermia due to blockage of spermatogenesis (Group 2).. Group 1 was divided into 38 eugonadotropes, 21 hypogonadotropes, and 13 hypergonadotropes; Group 2 consisted of 19 cases of blockage at the sperm acyte 2 or spermatide levels (Group 1a), 11 cases of blockage at the sperm ozonia or spermacyte 1 levels (Group 2a), and 10 cases of bilateral chrypt-orchidy of isolated Sertoli cells (Group 3a). 4 cases of Klinefelter's syndrome and 2 cases of testicular feminization wereaalso studied. Basal values of LH were significantly higher in Group 3a. After administration of 50 mcg of LH-RH iv, the LH values peaked after 20-30 minutes, except for Group 3a and the men with Klinefelter's syndrome and testicular feminization. The follicle stimulating hormone (FSH) basal values were significantly higher in Group 2. Maximum FSH values occurred 30-45 minutes after the LH-RH injection; the response took longer for hypogonadotropes and was very irregular in Group 3a and those with Klinefelter's syndrome. Prolactin levels of the patientswwere taken before and after administration of 200 mg of TRH iv. About 40% of the sterile men exhibited elevated prolactin levels before or after the injection. Testicular biopsies, semen analyses, and other parameters were measured. Of the cases where gonadotropin levels remained normal afte LH-RH administration, a pathological reason for sterility could be found for only 213 of the sterile men. Of the patients with low basal gonadotropin levels or weak response to LH-RH, 1/2 had diabetes or hemochromatosis. Of the patients who had strong LH responses and normal FSH responses to LH-RH administration, 1/2 had elevated prolactemia. A correlation between prolactin secretion and androgen secretion and a negative correlation between prolactinemia and the number of sperm/ml were found.
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PMID:[Investigation of the gonadotrophins and prolactin in sterile men (the LH-RH + TRH test) (author's transl)]. 41 78

Recently, evidence has been reported to suggest that human platelets like several other circulating blood cells may bind insulin. To examine whether human platelets contain specific insulin receptors, washed human platelets suspended in Hepes buffer were incubated at 24 degrees C with 125I-insulin in the presence and absence of unlabeled insulin and specific insulin binding was determined. Insulin binding by platelets increased progressively with time of incubation to reach a maximum at 3 h and was proportional to the number of platelets in the incubation mixture. Maximum insulin binding was observed at pH 8. Insulin degradation by platelets as assessed by TCA precipitability and reincubation studies was minimal. Scatchard analysis of the binding data and dissociation studies revealed evidence of negative cooperativity of the platelet insulin receptor. A high affinity dissociation constant of approximately equal to 3 X 10(9) M-1 was determined and the concentration of platelet insulin receptors was estimated as 25 binding sites/micron2 platelet surface area. Binding of 125I-insulin by platelets was inhibited by unlabeled porcine insulin and to a lesser extent by catfish insulin and porcine proinsulin but not by glucagon, prolactin, growth hormone, and thrombin. The findings indicate that human platelets contain specific insulin receptors. The significance of the platelet insulin receptor, particularly with respect to altered platelet function in diabetes mellitus, remains to be determined.
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PMID:Demonstration and partial characterization of insulin receptors in human platelets. 44 28

Consideration given to the literature data about the diabetogenic effect of prolactin, the basal prolactin secretion was investigated in 98 patients with diabetes mellitus. A significantly increased basal prolactin level was established. The influence of age, sex, disease duration, type of diabetes, blood sugar level, mode of treatment and vascular complications upon prolactinemia was studied. Significantly higher prolactinemia was found in insulin treated patients and insignificantly -- in diabetics with retinopathy. The correlation of prolactinemia with glycemia, insulinemia and lipacidemia is low. That provides gounds to admit that hyperprolactinemia plays no essential role as an additional diabetogenic factor in the patients with diabetes mellitus. The causal relationship between hyperprolactinemia and diabetes still remains not well elucidated.
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PMID:[Basal prolactin secretion in diabetes mellitus]. 51 54

Increased growth hormone and prolactin contents of the rat adenohypophysis during the development of experimental diabetes were found by colorimetric studies of stained electrophoregrams. 4 to 5 days after alloxan administration the levels of somatotropic hormone (STH) and prolactin were higher in comparison to those in intact animals by 58% and 43%, respectively. Experiments on the primary cell culture using the precursor 14C-L-leucine revealed an enhanced secretion of somatotropic hormone and prolactin by cells of the rats with alloxan diabetes. A possible role of the adenohypophyseal changes in the development of experimental diabetes is discussed.
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PMID:[Changes in somatotropic and lactotropic functions of the adenohypophysis of rats with acute alloxan diabetes]. 54 Jan 38

In labile diabetes mellitus wihout ketoacidosis we have studied plasma prolactin levels and a possible causal connection between fluctuation in blood glucose concentration and plasma prolactin, growth hormone and cortisol levels. The hormone concentrations in plasma and blood glucose concentration were determined at 20 min intervals for a 24 h period in six male patients with insulin treated diabetes mellitus. Prolactin varied within the normal range but without any significant rise in relation to sleep in five out of the six patients. Growth hormone levels were low with superimposed secretory peaks. Plasma cortisol showed a normal diurnal rhythm. Blood glucose fluctuated as expected, but the variations and especially the falls in blood glucose to non-hypoglycaemic levels were not followed by increases in plasma hormone concentrations. No relationship could be demonstrated between the changes in the plasma concentration of prolactin, growth hormone and cortisol.
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PMID:Diurnal variations in plasma prolactin, growth hormone, cortisol and blood glucose in labile diabetes mellitus. 55 82

In order to identify prolactin-producing tumours in human pituitary glands, 45 chromophobe adenomas, obtained from unselected necropsies, have been studied by various staining procedures including the immunoperoxidase technique for the demonstration of prolactin. The presence of immunoreactive prolactin was revealed in the cytoplasm of the tumour cells in six cases (13%), indicating that the occurrence of prolactin-producing adenomas is not rare. No correlations were established between tumours and clinical history. Two adenomas were detected in female and four in male patients. The age of the patients at necropsy ranged from 28 to 75 years. Three adenomas were associated with disseminated carcinoma, two with fatal liver disease, and one with diabetes mellitus, atherosclerosis, and pyelonephritis. Manifest endocrine symptoms were not disclosed, and endocrine investigations, including measurements of blood prolactin levels, were not undertaken. Thus, direct evidence is lacking as to whether or not these tumours were actively secreting prolactin. In the non-tumorous parts of the anterior lobes the number of prolactin cells was decreased in two cases, suggesting that prolactin released from the adenoma cells suppressed prolactin production in the non-tumorous pituitary. However, the number of prolactin cells of the non-tumorous adenohypophysis seemed to be unchanged in two and increased in another two cases. The present findings conclusively proved the existence of the prolactin-producing adenomas as a distinct entity. These tumours do not stain with acid or basic dyes, they are PAS or thionin negative, and do not contain immunoreactive growth hormone. Thus, by conventional staining procedures they are indistinguishable from other chromophobe adenoma types. Herlant's erythrosin and Brookes' carmoisine methods, claimed spedifically to stain prolactin cells, failed to provide reliable results, hence their use cannot be recommended in tumour identification. Immunoperoxidase staining of prolactin is the only technique which conclusively reveals the presence of immunoreactive prolactin in the cytoplasm of the tumour cells and permits diagnosis. It is proposed that this technique be introduced in pituitary morphological studies. Its application may lead to a better understanding of problems related to prolactin-producing tumours and their secretory activity.
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PMID:Localization of prolactin in chromophobe pituitary adenomas: study of human necropsy material by immunoperoxidase technique. 77 66

Serum prolactin values in normal pregnant women showed a progressive increase from a mean value of 50 ng/ml in the 12th week to 270 ng/ml at term, with the range at term being 100-600 ng/ml. There was a fairly good correlation (r = 0.7) between the values of 24-hour urine estriol in 138 determinations and in the serum prolactin in 133 pregnant women. The regression lines of serum hPRL values with time of gestation in cases of intrauterine growth retardation (IUGR) and diabetes mellitus were less steep than those seen in normal pregnancy. The serum hPRL value of patients with preeclamptic toxemia, latent diabetes, premature rupture of membranes, or multiple pregnancies were found not to differ significantly from the values observed in normal pregnancy. The results indicate that prolactin determinations in pathologic pregnancies are not useful as an aid in their evaluation.
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PMID:Serum prolactin in normal and pathologic pregnancy. 90 61


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