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)

Glycemia, growth hormone level and urinary catecholamine excretion were studied in 182 patients suffering from insulin-dependent diabetes mellitus during insulin therapy alone, and in 33 during treatment with insulin plus alpha- and beta-adrenoblockers. Under the effect of alpha-adrenoblockers glycemia proved to fall in the insulin-dependent patients, without increasing the insulin dose. The STH level diminished in these patients under the effect of alpha-adrenoblockers, even when glycemia persisted at the same level. But beta-adrenoblockers aggravated decompensation and the STH level remained unchanged. alpha and beta-adrenoblockers decreased the urinary adrenaline excretion and elevated noradrenaline, dophamine and DOPA excretion, irrespective of blood glycemia. The authors recommend the use of alpha-adrenoblockers to prevent the necessity of a considerable elevation of insulin doses during compensation in patients with the insulin-resistant form of diabetes mellitus. beta-adrenoblockers are not recommended in diabetes mellitus.
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PMID:[Effect of alpha and beta receptor blockaders on the degree of glycemia, growth hormone content of blood and catecholamine excretion in insulin-dependent diabetes mellitus]. 3 98

The sympathetic nervous system is of major importance for the regulation of several physiological functions. Drugs which inhibit the actions of catecholamines and adrenergic drugs are used in the treatment of many clinical disorders. The potential role of catecholamines in a number of human diseases has, however, until recent years been studied to a limited extent only due to lack of methods for quantitation of sympathetic nervous activity. After the development of enzymatic isotope-derivative assays, reliable measurements of noradrenaline and adrenaline in plasma became available. Studies in man have shown that plasma noradrenaline is an index of sympathetic nervous activity. The present survey deals with sympathetic nervous activity and plasma adrenaline in a number of clinical disorders viz. arterial hypertension, duodenal ulcer, thyrotoxicosis, diabetes mellitus and ketotic hypoglycemia.
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PMID:The role of catecholamines in clinical medicine. 10 29

The sensitivity of alpha- and beta-adrenergic receptors, and the antilipolytic actions of prostaglandin E1 or insulin on adipose tissue of obese diabetic and non-diabetic subjects have been studied. Accumulation of cyclic AMP in adipose tissue and release of glycerol in response to several catecholamines (adrenaline, noradrenaline and isoprenaline) in the presence or absence of an alpha-adrenergic blocker (phentolamine) have been used to assess catecholamine receptor sensitivity. No differences in beta-receptor activity were observed between diabetics and non-diabetics, either on glycerol release or accumulation of cyclic AMP; alpha-receptor activity was also similar, except for significantly less accumulation of cyclic AMP in diabetic tissue incubated with noradrenaline and phentolamine (p less than 0.01). The antilipolytic action of prostaglandin E1 (at concentrations of 30 fM to 30 pM) on lipolysis (stimulated submaximally with isoprenaline, 10(-7) M) was similar in diabetic and control groups. The antilipolytic action of insulin (from 10(-10) to 10(-6) M) on lipolysis was also similar between the groups. It is concluded that neither disorders of the catecholamine receptor nor of the antiliolytic actions of prostaglandin E1 or insulin are responsible for the abnormalities of fatty acid metabolism in adult diabetes.
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PMID:Catecholamine receptor sensitivity and the regulation of lipolysis in adult diabetes. 18 98

Subcutaneous adipose tissue was obtained from 9 patients with untreated diabetes mellitus and from 13 obese nondiabetics. After incubation with isoprenaline or noradrenaline, glycerol release and tissue cyclic AMP (cAMP) were determined. Basal glycerol release was twice as rapid from the diabetic adipose tissue. With isoprenaline, the cAMP concentration and the glycerol production was significantly higher in the diabetic adipose tissue. Noradrenaline did not increase glycerol production or cAMP concentration in the diabetic adipose tissue. Subcutaneous adipose tissue was also removed from the diabetics after antidiabetic treatment. Basal lipolysis was significantly reduced and noradrenaline significantly increased both glycerol release and cAMP production. With isoprenaline, cAMP production and glycerol release were significantly less after antidiabetic treatment than in the untreated state. The data provide evidence for increased alpha- as well as beta-adrenergic receptor sensitivity in human subcutaneous adipose tissue of untreated diabetic patients.
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PMID:Abnormalities in the adrenergic control and the rate of lipolysis in isolated human subcutaneous adipose tissue in diabetes mellitus. 18 19

The in vitro relationship between fat-cell size, glycerol release, and peak concentration of cyclic AMP was investigated in human adipose tissue obtained from 25 obese nondiabetic patients before and after a 7-day fast and from 23 patients with untreated diabetes mellitus. In the obese nondiabetic patients there was a linear correlation between fat-cell size and cyclic AMP concentration, and fat-cell size and the rate of lipolysis. This was found both in nonfasting and fasting nondiabetic patients. However, in diabetes mellitus, there was only a relationship between cell size and cyclic AMP concentration. The alpha-adrenergic and beta-adrenergic activity in human adipose tissue was assessed by comparing the effect of isoprenaline and noradrenaline on the cyclic AMP concentration. The activity of both receptors was found to be increased in fasting obese patients and in diabetics. In both conditions the alpha-adrenergic response to catecholamines predominated in small fat cells, whereas in large ones the beta response predominated. The results suggest that during fasting and in diabetes mellitus there is a correlation between fat-cell size and the responsiveness of the adrenergic receptors. Thus, catecholamines may be involved in regulating the fat-cell volume. The view is expressed that the abnormal catecholamine-induced lipolysis is solely due to changes at the level of the adrenergic receptors during fasting, whereas in diabetes mellitus the sequentional activation of lipolysis is disturbed at deeper sites as well.
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PMID:Relationship between lipolysis, cyclic AMP, and fat-cell size in human adipose tissue during fasting and in diabetes mellitus. 21 83

The rate of insulin, glucagon, and somatostatin secretion was measured from isolated rat islets maintained in a perifusion system. The effect of norepinephrine (NE) was simultaneously determined on the release rate of all three hormones. Norepinephrine was employed at an acute dose of 10 micrometers and in graded doses from 1 nM to 10 micrometers in the presence of high (22 mM) and low (1.4 mM) glucose conditions, insulin secretion was maximally inhibited at 10 micrometers NE concentration and was significantly depressed at 100 mM NE concentration. Under both high and low glucose conditions, glucagon release was maximally stimulated at 10 micrometers NE concentration and was significantly elevated at 10 nM NE concentration. Under high and low glucose conditions, somatostatin release was inhibited by 10 micrometers NE concentration and was significantly depressed at 100 nM NE concentration. During the initial maximal stimulation of glucagon, NE inhibition of somatostatin and insulin was prevented, possibly by the high level of glucagon released. A paracrine effect of glucagon on beta and delta cells is proposed.
Diabetes 1979 Oct
PMID:Effect of norepinephrine on insulin, glucagon, and somatostatin secretion in isolated perifused rat islets. 38 55

Twenty four hours' urinary excretion of catecholamines was examined in 30 children suffering from diabetes and in 30 healthy children. The results showed that in children suffering from diabetes, excretion of adrenaline was increased and that of noradrenaline decreased when compared with healthy children. Taking into consideration changes in the sympatho-adrenergic system activity in cases with different degrees of compensation of metabolic processes during insulinization, it should be stressed that in children with ketoacidosis, excretion of catecholamines was still different in comparison with control group. On the other hand in children with compensate diabetes after insulin therapy, that differences were little. Marked increase in free adrenaline excretion observed in children with ketoacidosis and its normalization by effective insulinization seems to support the diabetogenic and ketogenic role of this neurohormone. Decrease in free noradrenaline excretion in children suffering from juvenile diabetes appears to suggest that there is a diminished sensitivity of the sympathetic system resulting probably from specific autonomic neuropathy accompanying this disease.
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PMID:[Excretion of catecholamines in juvenile diabetes mellitus]. 39 57

The concentrations of catecholamines and the activities of dopamine-beta-hydroxylase were measured in blood obtained from decapitated diabetic and aged-matched control rats. The activity of dopamine-beta-hydroxylase in blood from diabetic rats was much greater (5 fold) than that seen for control rats. For both diabetic and control rats, decapitation was accompanied by an increase in levels of adrenaline and noradrenaline with no change in the activity of plasma dopamine-beta-hydroxylase. The results are consistent with a predominantly adrenal origin of catecholamines and extra-adrenal origin of dopamine-beta-hydroxylase. The high activity of dopamine-beta-hydroxylase in diabetes indicates either an increased activity of the sympathetic nervous system or changes in dopamine-beta-hydroxylase turnover.
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PMID:Adrenal origin of plasma catecholamines after decapitation: a study in normal and diabetic rats. 69 80

In Europe, about 1% of the women using oral contraceptives develop hypertension. Predisposing factors seem to be age, hypertension problems in past pregnancies, family history of hypertension, personal histories of kidney disorders, diabetes mellitus or adipositas, or diastolic pressure over 80 mm Hg. An overactive renin-angiotensin-aldosterone system may be an important factor in the etiology of this type of hypertension. Oterh possible factors are: reduced excretion of angiotensin 2, increased sensitivity of the arterioles to substances such as angiotensin 2 and noradrenaline, direct effect of ethinyl estradiol and mestranol on the sodium and water system, cardiovascular changes, disorders in the adrenergic system (e.g., catecholamine metabolism). Blood pressure should be checked before beginning any treatment with oral contraceptives and every 3 months after that. For the purpose of differential diagnosis angiotensin 2 in the plasma and catecholanin and its by-products should be checked (24-hour urine samples). In cases of serious hypertension hormone therapy should be discontinued at once. Primary aldosteronism and renal artery stenosis must be excluded in the differential diagnosis, for although these hypertensive disorders exhibit similar biochemical changes, they should be treated by surgical intervention. Usually hypertension is reversible after cessation of therapy with contraceptive steroids. However, some cases of irreversible hypertention, kidney failure, and malignant nephrosclerosis have been described. Hypertensive somen who wish to use oral contraceptives may, under medical supervision try a modified hormonal contraceptive (minipill without estrogen) or sequential or lower dosages.
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PMID:[Clinical aspects of hypertension under contraceptive steroids]. 79 66

1. The regulation of the synthesis of phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) in epididymal adipose tissue, liver and kidney in vivo was studied immunochemically. 2. Phosphoenolpyruvate carboxykinase (GTP) synthesis in adipose tissue is increased by starvation, diabetes and noradrenaline, and decreased by re-feeding and insulin. These changes were also seen in adrenalectomized rats and are qualitatively similar to those observed for the liver enzyme. This indicates the involvement of cyclic AMP as an inducer and insulin as a de-inducer in the regulation of phosphoenolpyruvate carboxykinase (GTP) in both tissues. (Induction and de-induction are defined as selective increase and decrease respectively in the rate of enzyme synthesis, regardless of the mechanism involved.)3. Adrenalectomy had little effect on phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney, but increased the synthesis rate of the adipose-tissue enzyme. Starvation and adrenalectomy had additive effects in increasing the synthesis rate of adipose-tissue phosphoenolpyruvate carboxykinase (GTP). In adrenalectomized diabetic rats glucocorticoids increased phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney while decreasing enzyme synthesis in adipose tissue. De-induction of adipose tissue phosphoenolpyruvate carboxykinase (GTP) is therefore regulated independently by glucocorticoids and insulin. 4. Although liver, kidney and adipose-tissue phosphoenolpyruvate carboxykinases (GTP) are seemingly identical, there is an apparent tissue-specific differentiation in regulatory systems for the enzyme.
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PMID:Regulation of phosphoenolpyruvate carboxykinase (GTP) in adipose tissue in vivo by glucocorticoids and insulin. 96 85


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