Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An equally lowered insulin specific binding in the fatty cell plasmic membranes was found in patients with glucocorticoid, somatotropin and catecholamine hyperproduction during diabetes mellitus and/or its absence. This fall is due exclusively to a reduced amount of binding sites in patients with hypercorticism and acromegaly, accompanied or not by diabetes, and in persons with diabetes-aggravated pheochromocytoma. The above decrease is caused by a lowered binding site number and augmented negative cooperativity in patients suffering from pheochromocytoma without diabetes. The results obtained allow a conclusion that inhibited expression of insulin receptors in the presence of counter-insulin hormone hyperproduction promotes diabetes arising.
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PMID:[Fatty tissue insulin receptors in patients with an elevated level of contrainsulin hormones with and without concomitant diabetes mellitus]. 638 48

Human pancreatic growth hormone releasing factor [GRF(1-44)] is the largest molecule of several peptides recently isolated from pancreatic tumours associated with acromegaly. It has been shown to stimulate the release of growth hormone in normal subjects and provides a safe and reliable tool for examining growth hormone release. A study was conducted to examine the release of growth hormone in patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes. GRF(1-44) stimulated the release of growth hormone in normal subjects and produced no side effects. A response of similar magnitude occurred in Type 1 diabetic patients despite their concomitant hyperglycaemia. In contrast, the response in Type 2 diabetes was significantly impaired compared with normal volunteers (p less than 0.05) and Type 1 diabetic patients (p less than 0.02). These findings may well indicate that there is a defect in central hormonal control in Type 2 diabetes.
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PMID:Impaired growth hormone response to human pancreatic growth hormone releasing factor [GRF(1-44)] in type 2 (non-insulin-dependent) diabetes. 643 89

Echocardiography was performed in 14 patients with acromegaly in order to characterize cardiac involvement in this disease. The left ventricle was enlarged or hypertrophic in 10 patients (71%): the fraction of myocardial shortening, an index of left ventricular contractility, was normal in all but one; and 10 patients had a reduced mitral EF slope, suggesting that their left ventricular compliance was reduced. Cardiac disease was not suspected clinically as most patients had normal clinical, ECG and X-ray examinations of the heart. Left ventricular hypertrophy occurred in the absence of hypertension, diabetes or evidence of coronary artery disease. There was a positive correlation between left ventricular wall thickness and duration of acromegaly but not between the former and growth hormone levels after fasting, suggesting that ther must be prolonged hypersecretion of growth hormone, and not simply high levels, before cardiac hypertrophy develops.
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PMID:The heart in acromegaly: correlation of echocardiographic and clinical findings. 644 20

The authors reviewed 102 cases of bilateral renal enlargement seen on excretory urography (excluding hydronephrosis and duplex kidneys) to determine the clinical significance of this finding. Associated abnormalities were found in 48 patients, including diabetes mellitus in 29; nondiabetic obesity, large body structures, or chronic steroid use in 16; acromegaly in 1; and unknown etiology in 37, 2 of whom were found to have diabetes five years later. Because of the striking preponderance of diabetes in this study, a fasting blood glucose analysis is recommended for patients with unexplained bilateral renal enlargement on excretory urography.
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PMID:Diabetes mellitus: the predominant cause of bilateral renal enlargement. 648 64

The interaction of insulin with its receptor represents one of the key intermediate steps between secretion of insulin and its final biologic effects. Alterations in this interaction have been found in a number of disease states, including obesity, non-insulin-dependent diabetes mellitus (NIDDM), glucocorticoid excess, and acromegaly, as well as several rare forms of severe insulin resistance. The major factor regulating the receptor in obesity and NIDDM appears to be insulin. In obesity this alteration in normal regulation occurs secondary to overeating, whereas in the diabetic state the nature of the primary defect is uncertain. The role of the receptor in insulin resistance and methods for its evaluation are discussed.
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PMID:Role of insulin receptors in insulin-resistant states. 699 Jan 80

Eleven patients with active acromegaly resistant to conventional therapy were treated with bromocriptine for 15 (12--22) months by increasing the daily dose stepwise from 5 to 10--60 mg. A satisfactory response was achieved in all but one of the eight patients, in whom the mean diurnal level of serum GH was less than 50 ng/ml, whereas patients with grossly elevated serum GH levels responded poorly. In the longterm, no overall effects on glucose tolerance or plasma insulin (IRI) levels were observed but the chemical diabetes of three patients ameliorated in two. On the other hand, a dose-dependent acute suppressive effect of bromocriptine on plasma IRI response to oral glucose was observed, suggesting a direct effect of bromocriptine on the release of insulin from beta cells. Bromocriptine seems to be a good alternative in the treatment of patients with acromegaly who have not responded to conventional therapy.
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PMID:Bomocriptine treatment of patients with acromegaly resistant to conventional therapy. 699 53

Sixteen patients with clinically active acromegaly were investigated; four of these had insulin-independent diabetes mellitus. Those acromegalic subjects who were not diabetic exhibited excessive insulin responses to glucose and arginine stimulation. By contrast, plasma glucagon concentrations in these patients did not differ significantly from those in control subjects. Acromegalic patients who also had insulin-independent diabetes had a markedly reduced insulin response to glucose stimulation, while arginine-induced insulin secretion was relatively well preserved. Although there was a tendency for plasma glucagon concentrations to be higher in the diabetic than in the nondiabetic group of acromegalic subjects, this difference did not achieve statistical significance either in the basal state or during the glucose amd arginine infusion tests.
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PMID:Plasma glucagon and insulin concentrations in acromegaly. 699 31

The association of the Albright syndrome (polyostotic fibrous dysplasia of bone, hyperpigmented skin macules, and endocrine disorders) with acromegaly has been infrequently substantiated. The case of an 18-year-old girl with the classic Albright syndrome and acromegaly is described. The patient had a history of coarsening of acral and facial features, an insulin-resistant form of diabetes mellitus and elevated fasting growth hormone values. Neuro-endocrine studies demonstrated failure of growth hormone to suppress to less than 5 ng/ml during an oral glucose tolerance test, and the abnormal release of growth hormone upon injection of thyrotropin-releasing hormone. Although L-dopa failed to decrease growth hormone levels, bromocriptine produced a modest decline in growth hormone within two hours of ingestion. The patient had also experienced secondary amenorrhea with sub-normal follicle-stimulating-hormone (FSH) and luteinizing hormone (LH) levels, both of which demonstrated a prolonged sluggish response to an injection of gonadotropin-releasing hormone (GnRH); this response suggested hypogonadotropic hypogonadism, possibly on the basis of a tumor involving both pituitary and hypothalamus. Sellar polytomography demonstrated an enlarged sella with dorsal erosion and an asymmetric floor. Computerized tomography of the brain visualized a suprasellar mass extending into the hypothalamus. These findings suggest a hypersecretion of hypothalamic releasing factors, pituitary hormones, or both as an etiology for the endocrinopathy in this patient, and lend support to the theory that the endocrinopathies associated with the Albright syndrome result from over-production of hypothalamic-releasing hormones or autonomous secretion of pituitary hormones from an adenoma.
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PMID:The Albright syndrome associated with acromegaly: report of a case and review of the literature. 701 31

The clinico-hormonal course of acromegaly and the presence of the hyperlipemic syndrome were studied in relation to age, sex, associated hypothyroidism, diabetes, obesity and cardiovascular and atherosclerotic complications in 43 acromegalic patients (18 males and 25 females) of which 6 had received no treatment and 37 had been submitted 2 - 13 years to conventional roentgentherapy (31 cases), 90Y (5 cases) and hypophysectomy (1 case). Hyperlipemia (HLP), present in 24 acromegalic patients (55.8% of the cases) unrelated to age, was more frequent in women (64% as against 44% in males) and correlated with the clinico-hormonal evolution (GH greater than 20 mg) (60% of the cases), and associated hypothyroidism (79%), obesity (42%) and diabetes (25%). Of the hyperlipemic acromegalic patients, 62% had cardiovascular and atherosclerotic complications. The results of the study point to the need for a hypoglucidic, hypolipidic and associated treatment for hypothyroidism, diabetes and obesity in the prophylaxis of acromegalic atherosclerosis.
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PMID:The dyslipemic syndrome in acromegaly. 704 Dec 36

Acromegaly is very often accompanied by impaired glucose tolerance or a manifest diabetes mellitus, with increased immunoreactive insulin (IRI) levels whose response during oral glucose tolerance tests (OGTT) is quite often exaggerated. When the dopaminergic drug bromocriptine is administered to acromegalics, their elevated growth hormone (GH) levels very often decrease, their impaired glucose tolerance (as manifested in OGTT) improves and their exaggerated IRI response becomes more normal. Eighteen patients were treated with bromocriptine. They were followed-up repeatedly during their treatment of varying duration for up to 6 years. These results indicate that raised GH levels are not the only factor that impairs glucose tolerance in acromegalics. During bromocriptine administration, impaired glucose tolerance improved and abnormal IRI levels (OGTT) became more normal even without any decrease in the high GH levels. In non-diabetic acromegalics, when bromocriptine was administered, there was not only an average decrease in the elevated GH values during OGTT, but a normalization of increased IRI values as well, without any major change in the corresponding blood glucose levels. During insulin tolerance tests (ITT), after i.v. insulin, the IRI levels after 30 and 60 min were markedly higher in acromegalics on bromocriptine than in the same patients before its administration, without any significant change in the corresponding blood glucose values. In 2 diabetic acromegalics, bromocriptine administration re-established their lost ability to increase IRI levels during OGTT. This was accompanied by a marked improvement in their glucose tolerance. It is probable that bromocriptine decreases glucagon levels in acromegalics, or at least in some of them. It is suggested that bromocriptine could protect the beta-cells of acromegalics from "exhaustion'.
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PMID:Bromocriptine and glucose tolerance in acromegalics. 704 36


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