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

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 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

Norepinephrine, epinephrine, and dopamine concentrations were studied in the cardiovscular system of postmortem material obtained from six long-term diabetics and six control subjects. Norepinephrine concentration was considerably reduced in the cardiovascular system of the diabetic patients. The mean norepinephrine concentration in the apex of the heart, the radial artery, the posterior tibial artery, and the femoral artery in the diabetics averaged 6, 9, 12, and 20 per cent, respectively, of the corresponding mean values in the controls. Epinephrine was present in the cardiovascular system in the controls but in small amounts in comparision with norepinephrine. There was no correlation between the epinephrine and the norepinephrine concentrations in the tissue. In the diabetics the epinephrine concentration in the heart and in the arteries did not differ from the values obtained in the controls. The dopamine concentration averaged 11 per cent of the norepinephrine concentration in the cardiovascular system in the controls. There was a strong correlation between tissue concentrations of dopamine and of norepinephrine. In the diabetics the dopamine concentration was reduced, but relatively less than that of norepinephrine, and constituted 53 per cent of the norepinephrine concentration. It is suggested that the depletion of the norepinephrine stores in the heart in diabetic patients may in part be responsible for their reduced survival rate in acute myocardial infarction.
Diabetes 1976 Jan
PMID:Norepinephrine, epinephrine, and dopamine contents of the cardiovascular system in long-term diabetics. 124 67

The aim of this study was to clarify whether or not arachidonic acid metabolic disorders are caused by a substrate inavailability and whether such disorders might contribute to circulatory disturbances in the diabetic myocardium. Norepinephrine induced a decrease in the conductivity of both coronary arterial bed and myocardial microcirculation in alloxan-diabetic dogs. It was markedly (p less than 0.05) attenuated both by indomethacin and acetylsalicylic acid pretreatments indicating an imbalance among the vasoactive prostanoids in diabetes. TXA2 release from the diabetic coronary rings was found to be elevated and could be normalized after the blockade of vascular adrenoceptors by phentolamine (p less than 0.05). PGI2 synthesis was also enhanced by adrenergic blockade in the diabetic arterial rings. After pretreatment with 14C arachidonic acid, in order to measure substrate availability, the arachidonic acid metabolic rate was less in the diabetic coronary arteries than in healty vessels (p less than 0.05). Ten mumol/l norepinephrine decreased arachidonic acid metabolism in the presence of prelabelled substrate in the diabetic animals, compared to an increase observed in metabolically healthy dogs. Therefore diabetes appears to diminish arachidonic acid metabolism and uptake independent of adrenoceptors and to induce an imbalance between vasoconstrictor and vasodilator cyclooxygenase products, resulting in elevated TXA2 release controlled by adrenergic mechanisms which may contribute to an impairment in myocardial microcirculation.
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PMID:Disturbed lipid metabolism in diabetic coronary vessels. 132 Jul 34

The sympathetic nervous system may contribute to excessive hepatic glucose output in Type 2 (non-insulin dependent) diabetes mellitus and could be implicated in the interrelated problem of hypertension. The aim of these studies was to determine whether subjects with Type 2 diabetes had normal sensitivity (compared with age- and weight-matched non-diabetic subjects) to noradrenaline infusion (60 ng.kg-1.min-1 for 60 min) and to compare the responses with oral tyramine administration (800 mg), and psychological stress (using competitive computer games). Noradrenaline infusion caused significantly greater plasma glucose (mean increment 2.1 +/- 0.4 vs 0.6 +/- 0.1 mmol/l, p less than 0.005) and pressor responses (mean systolic increment 21 +/- 3 vs 11 +/- 1 mmHg, p less than 0.02) in the diabetic subjects. The excessive glycaemia was due to increased hepatic glucose output rather than reduced glucose disposal. Tyramine administration caused significantly increased hepatic glucose output and plasma glucose levels, but with similar responses in the diabetic and non-diabetic subjects; the pulse and pressor responses were also similar between the groups. The psychological stressor induced significant increases in pulse, blood pressure and non-esterified fatty acid levels in the combined group of subjects (p less than 0.01) but did not influence plasma glucose levels in either diabetic or non-diabetic subjects. We conclude that pharmacologically-induced sympathetic nervous stimulation can induce hyperglycaemia. Subjects with uncomplicated Type 2 diabetes have increased sensitivity to exogenous noradrenaline but may not hyperrespond to endogenous sympathetic activation.
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PMID:The effects of sympathetic nervous system activation and psychological stress on glucose metabolism and blood pressure in subjects with type 2 (non-insulin-dependent) diabetes mellitus. 139 78

Patients with insulin-dependent diabetes mellitus have an increased mortality and morbidity due to vascular complications. Nitric oxide from the vascular endothelium contributes to the control of normal vascular tone, and endothelial dysfunction has been implicated in the pathogenesis of diabetic vascular disease. In this study we have examined basal and stimulated nitric oxide-mediated vasodilatation in insulin-dependent diabetics and age- and sex-matched healthy controls. Drugs were infused locally into the brachial artery and forearm blood flow measured using venous occlusion plethysmography. Noradrenaline and NG-monomethyl-L-arginine produced similar reductions in resting forearm blood flow in healthy controls. However, in the diabetics, NG-monomethyl-L-arginine was significantly less effective than noradrenaline. Comparing between groups, the response to NG-monomethyl-L-arginine was also significantly less in the diabetics compared with the healthy controls. The response to sodium nitroprusside was significantly less in the diabetics compared with the healthy controls, whereas the responses to both acetylcholine and verapamil were the same in the two groups. The results provide evidence for an abnormality of basal nitric oxide-mediated dilatation in the forearm arterial bed of patients with insulin-dependent diabetes mellitus, and suggest that the vascular smooth muscle is less sensitive to nitric oxide.
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PMID:Inhibition and stimulation of nitric oxide synthesis in the human forearm arterial bed of patients with insulin-dependent diabetes. 146 3

Submaximal exercise provokes an abnormal elevation in albuminuria in type 1 (insulin-dependent) diabetes mellitus. Plasma catecholamines might be involved in this phenomenon by a renal vasoconstrictive effect. Twelve healthy subjects (Controls: albuminuria < 10 micrograms min-1), 13 normoalbuminuric type 1 diabetic patients (DNormo: albuminuria < 10 micrograms min-1) and 13 microalbuminuric type 1 diabetic patients (DMicro: albuminuria 10-200 micrograms min-1) performed a fixed bicycle workload (600 kpm for 20 min+urine collection 40 min post exercise). None of the patients suffered from autonomic neuropathy or hypertension. Fractional albumin clearance (FalbCl) rose in DNormo (p = 0.02) and DMicro (p = 0.01) but not in the Controls (p = 0.40). Basal plasma adrenaline and noradrenaline were not different in the three groups. The increments in noradrenaline were more pronounced in DNormo and DMicro than in Control (Controls < DNormo, p < 0.05; Controls < DMicro, p < 0.01). The changes in FalbCl were significantly correlated with the changes in noradrenaline (all subjects r = 0.65, p < 0.001). The increments in adrenaline were not different in the diabetic groups compared to the controls, and were not related to the changes in FalbCl. Multiple regression analysis showed that changes in plasma noradrenaline (p < 0.002) and in mean arterial pressure (p < 0.005) independently contributed to the changes in FalbCl (multiple r = 0.73). It is concluded that the exercise-induced plasma noradrenaline response is increased in normo- and microalbuminuric type-1 diabetic patients. Noradrenaline appears to contribute in the exercise-induced changes in renal protein handling, possibly by its effect on renal haemodynamics.
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PMID:Abnormal plasma noradrenaline response and exercise induced albuminuria in type 1 (insulin-dependent) diabetes mellitus. 148 18

The vascular smooth muscle contractile response to neuropeptide Y (NPY), potassium, noradrenaline, histamine and serotonin was studied in circular segments of isolated vessels in vitro from rabbits with alloxan-induced diabetes mellitus. The injection of alloxan resulted in a marked and maintained increase in serum glucose as early as 1 week after treatment. Four vessel types were examined: abdominal aorta, and renal, left anterior descending coronary and middle cerebral arteries. There was no difference in the contractile response to histamine or serotonin between control and diabetic vessels. However, in the cerebral artery the contractile response to noradrenaline was reduced in the diabetic group, while in the aorta and the renal artery no significant differences were seen. Noradrenaline failed to evoke any contractile response in the coronary arteries in either group. NPY induced strong, concentration-dependent contractions of coronary and cerebral arteries, but did not have any contractile effect per se in aorta or renal arteries, either in control or in alloxan-treated rabbits. The maximal contractile effect and the sensitivity to NPY was significantly less in diabetic coronary and cerebral vessels as compared to control. There was no difference in dilator effect of acetylcholine and substance P between the diabetic animals and the control group in any of the vessel types, indicating that the changed vascular responses to NPY and noradrenaline were not endothelium-dependent. In conclusion, the present study has shown that the postjunctional effects of NPY and noradrenaline in the peripheral sympathetic nervous system are selectively attenuated in this model of chronic diabetes.
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PMID:Diminished contractile responses to neuropeptide Y of arteries from diabetic rabbits. 158 98

This study was aimed at evaluating cardiac function, both systolic and diastolic, in young type 1 diabetics with a mean duration of the disease of 10.9 +/- 6 years and without evidence of cardiac autonomic neuropathy and micro- or macroangiopathy. Thirteen diabetics, with good metabolic control, and 10 normal matched subjects were studied by echocardiography at rest and by radionuclide ventriculography both at rest and during effort. The level of plasma catecholamines was also determined. The echocardiographic data were comparable in the two groups. Scintigraphic data showed an increased peak ejection and peak filling rate (P less than 0.001) in diabetics while the other indices of cardiac function were comparable. Norepinephrine (P less than 0.01) and epinephrine (P less than 0.001) were higher in diabetics. A hypothesis is formulated that the higher indices of flow velocities in type 1 diabetics are supported by a sympathetic overactivity.
Diabetes Res Clin Pract 1990 Jan
PMID:Cardiac function and sympathetic activity in young diabetics. 230 95

The influence of alloxan-induced diabetes mellitus on the sympathetic neuroeffector junction of the rabbit carotid artery denuded of endothelium was studied. Six weeks of diabetes resulted in a neuropathy characterized by a 38% reduction in the arterial content of norepinephrine. Norepinephrine release from the nerves measured from electrically stimulated superfused arterial segments was decreased. The cocaine-sensitive accumulation of [3H]-norepinephrine (NE) was also reduced, reflecting decreased neuronal uptake. The consequences of these prejunctional changes were studied by measuring isometric contractions of arterial rings caused by electrical nerve stimulation or by exogenous norepinephrine. Despite the reduced release of norepinephrine, neurogenic contractions were normal, suggesting an increased sensitivity of the smooth muscle. After neuronal uptake was blocked, the neurogenic contractions of diabetic arteries were less than normal, reflecting the reduction in transmitter release. The sensitivity of diabetic arteries to exogenous norepinephrine was increased under control conditions; maximal contractions were unchanged. Blockade of norepinephrine uptake increased norepinephrine sensitivity more in normal than in diabetic arteries, and there was no longer a significant difference in sensitivity. Thus, under control conditions, neurogenic contractions of the partially denervated diabetic rabbit carotid artery are paradoxically normalized by increased alpha-adrenergic sensitivity of the smooth muscle. The increased sensitivity caused by reduced neuronal uptake can thus preserve neurogenic vasoconstriction and cause supersensitivity to exogenous catecholamines in the sympathetic neuropathy caused by diabetes mellitus.
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PMID:Adrenergic denervation in rabbits with diabetes mellitus. 237 13


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