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

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Thirty patients with active acromegaly were divided into five groups according to the results of their IRI and blood glucose curves in the course of oral glucose tolerance test. Young acromegalics with short duration of acromegaly had grossly exaggerated IRI response with the peak in the first half-an-hour and the flat blood glucose curve. In the second group the peak of IRI response was in the first hour and the blood glucose curve rose to high values in the early stage after the glucose load. The IRI response in the third group was still exaggerated but delayed and the diabetic type of blood glucose curve was found in some of these patients. Acromegalics with overt diabetes mellitus lost their exaggerated IRI response and the IRI curves were flat in those with more advanced disturbance of glucose tolerance. It was suggested that the groups described might represent individual stages in the development of diabetes mellitus in acromegaly. Unclear position in this scheme is kept by the group of active acromegalics with IRI response in normal limits and glucose tolerance unimpaired.
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PMID:Insulin secretion and glucose tolerance in acromegaly. 100 8

Hypoglycaemic and growth hormone responses were studied at different steady-state plasma insulin concentrations during a graded infusion of monocomponent human insulin. The control group consisted of ten volunteer subjects. The other groups studied included women taking oral contraceptives and patients with obesity, thyrotoxicosis, myxoedema, acromegaly, diabetes mellitus (moderate and severe) and liver disease. The hypoglycaemic response was measured in two ways: (i) the percentage reduction in plasma glucose below basal, and (ii) the rate of fall of plasma glucose (Kg-%/min). Insulin sensitivity was greatest in the normal subjects and in the other groups decreased in the order thyrotoxicosis greater than oral contraceptive greater than obesity greater than myxoedema greater than acromegaly greater than liver disease. Insulin sensitivity was difficult to assess in the diabetic patients because basal plasma glucose concentrations were elevated. At any given insulin concentration, the diabetics metabolized approximately the same amount of glucose as the normal subjects but the fact that this rate of glucose turnover occurred at higher plasma glucose concentrations probably indicated insulin resistance. Within each group Kg at each dose level of insulin correlated with the steady state plasma insulin concentration during the same infusion period. Diminishing sensitivity to insulin was reflected in an increasing fasting plasma insulin and insulin/glucose ratio except in patients with diabetes. GH responses to insulin infusion in normal subjects reflected the pattern of fall of plasma glucose. In the diabetic patients GH secretion appeared to be related to the infusion of insulin and occurred before plasma glucose had fallen to hypoglycaemic levels. GH secretory patterns were within normal limits in women taking oral contraceptives and in seven of eleven patients with liver disease but were impaired in three of seven patients with thyrotoxicosis and four of five patients with myxoedema. Four obese patients had a markedly delayed but eventually normal GH response.
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PMID:Metabolic responses to monocomponent human insulin infusions in normal subjects and patients with liver and endocrine disease. 110 16

Oral administration of 1.0 or 2.5 mg bromocriptine (CB 154: 2-brom-alpha-ergocryptine) in nine of twelve patients with active acromegaly resulted in a reduction of growth hormone level by 80-90% over 8-10 hours. During treatment for 2-9 months with daily doses of 4.0 to 10.0 mg bromocriptine, there was a sustained reduction of growth hormone levels in these patients. At the same time soft-tissue swellings and tendency towards sweating decreased. In two patients with diabetes mellitus the blood sugar profile improved and in one of them the insulin dose could be markedly reduced. The rise in growth hormone levels after TRH administration also occurred during bromocriptine treatment. In those patients in whom growth hormone levels failed to react to either acute or chronic administration of bromocriptine no rise followed TRH administration. It is possible that in these patients there is a hypophyseal adenoma without hypothalamic control. On gradually increasing dosage bromocriptine was tolerated without side effects.
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PMID:[Therapy of acromegaly using bromocriptine]. 114 34

Experience in the management of 100 cases of acromegaly is described. Three quarters of these had been referred directly to the endocrine clinic at the Middlesex Hospital. The remainder were referred from the Royal Post-graduate Hospital because they were thought unsuitable for yttrium implantation. The patients were studied by clinical assessment of severity, by measurement of basal growth hormone levels on three separate mornings, and by a review of possible complications. Particular attention was paid to diabetes, hypertension, cardiomegaly, respiratory, vascular and skeletal changes as well as visual field defect. Aggressive treatment was recommended in 77 patients. It was not recommended in the remainder on account of age, intercurrent illness or the apparent mildness of the condition. Fifty-nine patients were treated by trans-sphenoidal hypophysectomy. In 46 of the 59 patients the mean basal growth hormone level has been reduced to 5 ng/ml or less. In 39 this followed operation, in five operation and subsequent X-ray therapy and in two operation and the continuing effect of previously implanted yttrium. Of these 46 patients in whom the growth hormone level has been reduced to normal, 26 do not show any deficiency of anterior pituitary trophic hormones, 13 have gonadotrophin defect (in eight of these it was present before the operation) and seven require full replacement therapy. One patient died at home six weeks after the operation from a pulmonary embolus. There was one case of CSF rhinorrhoea which stopped spontaneously and three of acute frontal sinusitis. Trans-sphenoidal hypophysectomy is shown to be an effective means of treating acromegaly. If the basal level of growth hormone is not reduced to normal by six weeks after operation, it is recommended that a course of X-ray therapy should be given. This does not apply if irradiation has been used before operation.
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PMID:The treatment of acromegaly with special reference to trans-sphenoidal hypophysectomy. 115 91

Degenerative joint disease (DJD) is characterized by pain on use. X-rays show cartilage narrowing and osteophytes. Synovial effusions are non-inflammatory, i.e. clear wiht good viscosity and less than 2000 WBC per mm. 3 Cartilage fragments may be seen in the joint fluid. Important systemic diseases that can cause degenerative joint disease include ochronosis, hemochromatosis, hyperparathyroidism, acromegaly, Ehlers-Danlos syndrome, diabetes and syphilis with their neuropathic joints, Wilson's disease and hypothyroidism. The late results of other diseases such as rheumatoid arthritis and aseptic necrosis may resemble DJD.
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PMID:Laboratory diagnosis of degenerative joint disease. 116 90

Two patients with acromegaly have been treated with hypophysectomy. Because the disease was still active, the patients were reoperated. No pituitary tissue could be found at the second operations. Besides the acromegaly, one of the patients had diabetes mellitus (appeared after the first operation), Cushing's syndrome, probably ACTH-dependent, and evidence of thyrotoxicosis. In both patients extopic pituitary tissue was suspected. One of the patients reacted with a normal fall in plasma growth hormone to growth hormone releasing-inhibiting hormone. Ectopic pituitary function should be suspected, if the pituitary function is retained after a hypophysectomy.
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PMID:Ectopic pituitary function. 118 87

The incidence and type of x-ray semeiotics of the skull involvement were studied in 703 patients with endocrine diseases (26 with acromegaly, 36 with hypercorticism, 104 with thyrotoxicosis, 23 with hypothyrosis, 98 with primary hyperparathyrosis, 302 with diabetes mellitus, 114 with hypogonadism). Craniogram analysis involved study of the thickness and structure of the vault bones, shape and size of the skull, status of the sutures, internal plate relief, changes of the base of the skull, of the sella turcica first of all, and facial bones. The characteristic x-ray symptom complexes of the involvement of the skull in some endocrine diseases were distinguished.
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PMID:[X-ray semeiotics of cranial involvement in endocrine diseases]. 130 8

1. The ability of glucose to suppress growth hormone (GH) secretion is well known and the glucose test is widely used for the diagnosis of acromegaly. However, when suspected acromegaly is associated with diabetes mellitus (DM) or impaired glucose tolerance (IGT) the interpretation of the GH response to the oral glucose tolerance test (OGTT) may be difficult. Recently, Hattori et al. (Journal of Clinical Endocrinology and Metabolism, 70: 771-778, 1990), using a highly sensitive (1.5 ng/l) polyclonal antibody-based immunoenzymometric assay, found no differences in the GH response to glucose load among control, IGT and DM patients. 2. We employed a less sensitive (100 ng/l) but monoclonal antibody-based immunoenzymometric assay to measure the serum GH levels of 19 normal subjects, 11 patients with DM and 11 patients with IGT to determine the effect of glucose intolerance on the GH response to the OGTT. 3. Complete suppression of GH (< 0.1 microgram/l) was achieved in 73% of the controls with a mean nadir of 0.17 +/- 0.16 microgram/l (range, < 0.1-0.6 microgram/l). GH was completely suppressed in 82% of the diabetics with a mean nadir of 0.58 +/- 1.21 micrograms/l (range, < 0.1-4.0 micrograms/l). However, complete suppression occurred in only 27% of the IGT patients with a nadir of 1.09 +/- 2.08 micrograms/l (range, < 0.1-7.0 micrograms/l), which was statistically higher than observed for controls and diabetics. 4. We conclude that plasma GH levels after glucose loading of IGT patients should be interpreted with caution because an abnormal response can be detected when some sensitive immunometric assays are employed.
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PMID:Do impaired glucose tolerance and diabetes mellitus interfere with the interpretation of the growth hormone response to the oral glucose tolerance test? 134 20

The insulin-like growth factor (IGF) family of peptides, binding proteins, and receptors are ubiquitous and important for normal human growth and development. Modern techniques including specific radioimmunoassays, radioreceptor assays and recombinant DNA technology have improved our understanding of the role of IGFs in growth and development. In addition to enhancing our understanding of normal physiology, these techniques assess changes in these hormones, binding proteins, and receptors in pathologic conditions including growth retardation, acromegaly, malnutrition, diabetes, and malignancy. Further, these studies have led to improvement in the assessment of responses to certain therapies used in the treatment of these diseases and may lead to improvements in these therapies.
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PMID:NIH conference. Insulin-like growth factors in health and disease. 146 41


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