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

We have previously noted increased platelet aggregation and high von Willebrand factor activity in patients with chemical diabetes. In this paper we have studied platelet aggregation, plasma glucose, insulin, free fatty acids, growth hormone, and von Willebrand factor activity during the glucose tolerance test in six normal and six chemical diabetic subjects. The results suggest that von Willebrand factor activity is suppressed coincident with the rise of glucose and insulin and provide further evidence of hormonal and metabolic control of levels of von Willebrand factor activity.
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PMID:The effect of oral glucose on von Willebrand factor activity in normal and diabetic subjects. 30 1

The effect of oral administration of carbamazepine for a period of three weeks on serum growth hormone, serum immunoreactive insulin, and blood glucose was studied in healthy volunteers using a levodopa stimulation test. Serum growth hormone rose significantly from 1.3 +/- 0.3 ng/ml to 16.3 +/- 3.4 ng/ml in 60 minutes after levodopa administration (1000 mg orally) before carbamazepine, and almost similarly from 2.3 +/- 0.5 ng/ml to 15.1 +/- 4.0 ng/ml after carbamazepine during the test. No consistent changes were found in blood glucose concentrations in the levodopa test before or after carbamazepine. Levels of serum IRI were also normal throughout the test and no impairment in insulin secretion was seen during carbamazepine treatment. It is suggested that carbamazepine does not lead to an altered anterior pituitary function or to an impairment in insulin secretion. This is of advantage when growing children or subjects with a risk factor for diabetes are treated.
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PMID:Secretion of human growth hormone and insulin in levodopa test during carbamazepine therapy. 32 Aug 26

Somatostatin, a peptide inhibitor of growth hormone release originally isolated from the hypothalamus, is also present in D cells of pancreatic islets. Its ability to inhibit the secretion of insulin and glucagon suggests that it may be a local regulator of pancreatic A- and B-cell function. Studies using synthetic somatostatin have provided evidence that glucagon is a physiologically important hormone that exacerbates the consequences of insulin deficiency in human diabetes mellitus. The ability of somatostatin to diminish both fasting and post-prandial hyperglycemia and to forestall the development of ketoacidosis after withdrawal of insulin in insulin-dependent diabetics suggests a potential therapeutic use of this agent in diabetes. Presently, however, its short half-life and diverse actions preclude such use and have prompted the search for more specific and longer-acting analogs.
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PMID:Somatostatin. Its possible role in carbohydrate homeostasis and the treatment of diabetes mellitus. 32 23

The prevailing concept of etiologic heterogeneity for the diabetes mellitus syndrome is one of multiple genetic factors interacting with a variety of environmental influences. Variation in expression of the disorder, particularly the need for insulin, does not correlate with known etiologic distinctions. There is much evidence for genetic heterogeneity, as well as phenotypic variation when etiology can be presumed to be identical. The vascular manifestations of diabetes include microangiopathy unique to diabetes and larger vessel disease that differs from that of normal aging only by its prematurity. There is as much evidence for heterogeneity of the vascular expression as there is for glucose intolerance. Approximately 25% of persons with insulin-dependent diabetes may never develop the microvascular disease. The pathogenesis of vascular disease in diabetes may involve a number of abnormalities of plasma, circulating cells, and vascular tissue. Were absolute control of glycemia possible, some of the contributing factors involved in vasculopathy would possibly be alleviated. In the absence of automated physiologic insulin replacement the potential deleterious effect of our current methods of treatment might be reduced by specific inhibition of excess catecholamine, growth hormone and/or glucagon responses.
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PMID:Nature and nurture in the expression of diabetes mellitus and its vascular manifestations. 33 1

Bromocriptine, a long acting dopamine agonist, has been used to treat 73 patients with active acromegaly for between 3 and 25 months. Clear clinical improvement occurred in 71 patients (97%). This included improvement in facial appearance, reduction in hand and foot size and sweating, relief of headaches and increased energy and libido. Abnormal visual fields became normal in two patients, but one of these was given concomitant radiotherapy. A significant reduction in growth hormone occurred in 58 patients (79%), but only 15 patients had levels persistently below 5microgram/l. Carbohydrate tolerance improved with the reduction in growth hormone and of 23 patients with diabetes mellitus before treatment, glucose tolerance became normal in 15 and improved in a further 5. Administration of bromocriptine should begin slowly in order to minimise early side effects. Long term side effects have been minor to date and the deaths of two patients whilst taking the drug were not considered to have been caused by it. Bromocriptine offers a major advance in the management of acromegaly, but further careful follow-up is required to determine whether serious side effects will be a problem with the long term use of high doses.
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PMID:Acromegaly--results of long term treatment with bromocriptine. 34 61

Plasma insulin responses to a 4-hour glucose tolerance (100 g) were studied in urbanized Black people. Persons of normal weight without diabetes (12) and obese persons without diabetes (18) were compared with obese diabetics (19). Fasting serum ketone levels were measured, and the plasma potassium, triglyceride and growth hormone responses during the glucose tolerance test were determined. Obese subjects without diabetes had a twofold greater total plasma insulin response (area under curve) than their counterparts of normal weight, but there was a progressive fall in total plasma insulin response from subjects with mild diabetes (with fasting normoglycaemia) to those with severe diabetes (with fasting hyperglycaemia). The early plasma insulin responses of the group with mild diabetes were significantly impaired, and the peak response was only reached at 120 minutes. The subjects with severe diabetes had a flat insulin response curve. Fasting serum ketone levels were highest in the group with severe diabetes. The growth hormone responses were similar in all the groups. Plasma potassium and tryglyceride levels fell less during the glucose tolerance test in the group with severe diabetes than in the other three groups. These data indicate that insulin secretion is reduced in obese Blacks with chemical evidence of diabetes and this reduction becomes severe in the symptomatic diabetic.
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PMID:Hormonal and metabolic responses to an oral glucose load in obese Black diabetics. 35 29

We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. These facts may one day provide a rationale for therapeutic efforts to suppress excess glucagon secretion in the management of diabetes in man.
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PMID:Glucagon and diabetes. 35 37

Nineteen insulin dependent diabetics with onset at 30 years of age or less and duration of diabetes of greater than 25 years were divided into two groups on the basis of the presence or absence of clinically evident vascular disease. The patients without vascular disease were characterised by a later mean age of onset, lower fasting growth hormone concentration, and a lower frequency of the unusual HLA pattern B8 without A1 compared to the diabetics with vascular complications. The level of blood glucose control assessed over the last 15 years, insulin antibody titres, plasma glucagon levels and plasma cholesterol did not differ between the two groups. Residual beta cell activity was found in only one of the 19 patients. Although this study does not exclude an effect of the degree of blood glucose control or persistence of beta cell function in the early stages of diabetes on the subsequent development of vascular disease, it suggests that genetic factors, age of onset and plasma growth hormone levels may be more important.
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PMID:Hormonal profile, blood sugar control and HLA patterns in long-term insulin dependent diabetes with and without vascular disease. 36 9

The AA. have investigated the relationship between the secretion of GH and diabetic angiopathy a group of 17 subjects with chemical diabetes during a standard dexamethasone os i.v. glucose test. The results show that functional subclinical microangiopathy was present in the majority of the diabetics studied, who also showed an exaggerated growth hormone response to glucose. Thus, these results suggest that a positive correlation exists between alterations in the secretion of growth hormone and the development of diabetic microangiopathy.
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PMID:[Vascular alterations and GH secretion in latent chemical diabetes]. 39 51

In twenty-two patients with active acromegaly who were untreated or unsuccessfully operated or irradiated (mean growth hormone (GH) values greater than 4 ng/ml) the following investigations were performed: routine laboratory tests, tomography of pituitary fossa, oral glucose tolerance tests, TRH and other pituitary function tests and GH profiles over 5-10 h before and during bromocriptine treatment with daily doses between 7.5 and 50 mg. In seventeen patients GH was suppressed to less than 50% by bromocriptine, in thirteen of them it was normalized on at least one occasion. A TRH induced GH release was observed in all but two responders to bromocriptine before therapy. This effect of TRH was not blunted during treatment with bromocriptine and also in the two patients with negative tests before therapy a significant GH increase was observed. In no non-responder to bromocriptine was a significant increase of GH after TRH observed. One patient showed a secondary resistance to bromocriptine during a period of treatment with griseofulvin. In the remaining sixteen patients the GH suppression has been consistent for between 3 and 22 months. A single dose of pimozide abolished the bromocriptine effect on GH totally in one patient; in others a slight or no significant effect was observed. Tissue swelling and sweating decreased in all bromocriptine responders and glucose tolerance improved in five patients. In four diabetic patients a partial or full remission of diabetes occurred. Apart from postural hypotension after the first administration in two patients no other severe side effects have been observed. Sella size and the other pituitary functions did not change during the time of the study. It seems that a high percentage of acromegalics may be successfully treated with bromocriptine.
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PMID:Metabolic and clinical studies on patients with acromegaly treated with bromocriptine over 22 months. 40 54


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