Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Norepinephrine was infused for 60 minutes in high physiological concentration (0.08 microgram/kg/min) into seven insulin dependent diabetic subjects with no demonstrable endogenous insulin secretion and into seven normal subjects. Insulin dependent diabetic subjects had a stable, free insulin concentration of 23 +/- 5 microunits/ml which was unaffected by norepinephrine infusion. In the normal subjects, norepinephrine induced an initial inhibition of insulin secretion which lasted for approximately 20 minutes. Norepinephrine infusion caused a rapid increase in both ketone body and glucose concentrations but this response did not differ between the two groups. In contrast, plasma nonesterified fatty acid and triglyceride concentrations were increased significantly more in the normal than in the diabetic subjects. The increase in plasma glucagon concentrations was similar in the two groups of subjects. The cause of the differential metabolic response to norepinephrine between the normal and diabetic groups was not resolved, but may be related, at least in part, to suppression of endogenous insulin secretion in the normal subjects.
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PMID:The metabolic response to norepinephrine in normal versus diabetic man. 72 Jul 76

The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. Plasma catecholamine and PP levels rose in both groups in response to hypoglycemia and the secretory response of ACTH was lower in the diabetic subjects (p < 0.01). GRP concentrations increased during hypoglycaemia (p < 0.01) while a reduction in AVP occurred at the start of hypoglycaemia (p < 0.001). The plasma AVP concentrations were higher in the diabetic group compared with those in the normal group (p < 0.05). The NPY concentrations were higher in the normal subjects (p < 0.05) but no change in the mean level occurred in either group during hypoglycaemia. No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. These observations support the view that regulatory peptides, if involved in glucose homeostasis, may rather have a modulatory effect than a direct action in restoring normoglycaemia.
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PMID:The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man. 128 60

The effects of Type 1 diabetes mellitus and of exposure to mainstream cigarette smoke on noradrenaline (NA) uptake and its subsequent metabolism by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) in the perfused lungs of rats were examined. In diabetic (streptozotocin-treated) rats, there was an increase in the metabolic clearance of NA in the lungs, and this appeared to be due to the observed increase in NA uptake. During acute exposure of rat lungs to cigarette smoke, there was again an increase in the metabolic clearance of NA, and this was not due to any increase in the activity of either COMT or MAO, but we have not yet investigated whether it is due to an increase in NA uptake. After prolonged exposure of rats to cigarette smoke (daily for 3 months), NA uptake in the lungs was increased, but there was no change in the activity of either COMT or MAO. The results suggest that increased pulmonary clearance may reduce the elevated plasma catecholamine levels that have been described both in patients with Type 1 diabetes mellitus and in cigarette smokers.
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PMID:The effects of type 1 diabetes mellitus and of tobacco smoke on dissipation of catecholamines in pulmonary endothelial cells--a non-neuronal site of uptake1. 184 Jan 12

In order to find out objective indices for "hidden" hypoglycemia in diabetic patients the urine excretion of the catecholamines adrenaline, noradrenaline, dopamine and the serum levels of cortisol and somatotrophic hormone (STH) were followed up. 45 diabetics on insulin treatment were included in the study: 32 patients with type I diabetes mellitus and 13 patients with diabetes mellitus type II with secondary resistance to sulfanilurea drugs and insulin. The patients were classified into the following groups: I. without hypoglycemia--28 patients; 2. with diurnal hypoglycemia--6 patients and 3. with nocturnal hypoglycemia--II patients. In the patients with hypoglycemia the 24 h adrenaline urine excretion was higher than in the patients without hypoglycemia. No such differences were found for noradrenaline and dopamine. The separate examination of the diurnal and nocturnal catecholamines excretion showed in all groups that they cannot serve as an objective index for determination of hypoglycemia. The STH showed no differences in all groups of diabetics. Disturbances in the circadian rhythm of cortisol secretion in diabetics were found. This could be a good and available marker for detecting "hidden" hypoglycemia in diabetics.
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PMID:[Catecholamine excretion in diabetics on insulin treatment]. 228 57

The plasma catecholamine response to a standardized bicycle exercise test was evaluated in 24 insulin-dependent diabetic (IDDM) patients in whom the heart rate reactions to deep breathing (E/I ratio) and to tilt, the immediate acceleration and the transient deceleration (acceleration and brake indices), had been assessed as tests of autonomic neuropathy. Patients with an abnormal acceleration index (n = 8) showed, compared with non-diabetic (n = 18) controls who had participated in previous studies, an impaired increment in noradrenaline during exercise (80% of maximal working capacity) (MWC) (12.38 +/- 1.46 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (50% of MWC: 0.25 +/- 0.04 nmol l-1 vs. 0.54 +/- 0.08 nmol l-1; P less than 0.05). Similarly, patients with an isolated abnormal brake index (n = 6), i.e. with a normal acceleration index and a normal E/I ratio, showed compared with controls an impaired increment in noradrenaline (9.53 +/- 1.66 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (1.41 +/- 0.22 nmol l-1 vs. 2.92 +/- 0.51 nmol l-1; P less than 0.05) during 80% of MWC. IDDM patients with abnormal heart rate reactions to tilt, an abnormal acceleration index or an abnormal brake index show impaired catecholamine responses to exercise, which can be demonstrated also in patients without signs of parasympathetic neuropathy.
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PMID:Impaired responses of plasma catecholamines to exercise in diabetic patients with abnormal heart rate reactions to tilt. 274 44

Insulin-dependent diabetes mellitus (IDDM) in humans is accompanied by an attenuation of the response of glucagon to hypoglycemia. To identify an animal model of IDDM with alpha-cell unresponsiveness to glucopenia in which to pursue morphologic and in vitro functional investigation of the lesion, pancreases isolated from rats with IDDM induced by streptozocin (STZ) or occurring spontaneously in BB/W rats were perfused with buffer containing 150, 25, and 150 mg/dl of glucose. In both forms of IDDM the normal glucagon rise during glucopenia was markedly impaired, suggesting an abnormality comparable to that of human IDDM. Studies of the insular sympathetic apparatus were conducted in these rat models. Electron-microscopic examination of peri-insular nerve endings disclosed no discernible abnormality in either form of rat IDDM. However, morphometric analysis of contacts between [3H]norepinephrine-labeled sympathetic nerve terminals and alpha-cells in pancreases from STZ-induced diabetic (STZ-D) rats revealed a 65-70% reduction in direct contacts. An 80% reduction in the number of nerve endings (not labeled) in direct contact with alpha-cells was also noted in the BB/W diabetic rats. Norepinephrine reuptake, studied only in the STZ-D group, was not impaired. The availability of local endogenous norepinephrine to alpha-cells and their sensitivity to exogenous norepinephrine was determined by perfusing 2, 5, or 10 micrograms/ml of tyramine, a releaser of endogenous norepinephrine, and norepinephrine at a concentration that in pancreases from nondiabetic rats gave a quantitatively similar glucagon response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphologic and functional changes in sympathetic nerve relationships with pancreatic alpha-cells after destruction of beta-cells in rats. 354 58

During constant insulin infusion (0.15 mU X kg-1 X min-1) from 12 PM to 8 AM in 10 IDDM patients previously rendered euglycemic (Biostator), plasma glucose (5.4 +/- 0.2 mmol/L at 12 PM) increased by 3:30 AM and reached 12.1 +/- 1.6 mmol/L at 8 AM (P less than 0.001). Glucose production also increased at 3:30 AM; hyperglycemia, glucose utilization did not increase until after 5 AM. Plasma growth hormone (12 PM to 4 AM), cortisol (after 3:30 AM), noradrenaline (after 1:30 AM), and adrenaline (after 3:30 AM) but not glucagon increased significantly overnight, although plasma adrenaline and noradrenaline remained at subthreshold levels. Insulin clearance increased (approximately 25%, P less than 0.05) but only after 7 AM, resulting in a 4 mU/L decrease in plasma insulin. A significant correlation was found between increases in plasma glucose and increases in glucose production (r = 0.74, P less than 0.05) which in turn were significantly correlated with nocturnal peaks in plasma growth hormone (r = 0.66, P less than 0.05). From the sequence of events observed, we conclude that the Dawn Phenomenon in IDDM begins earlier than is currently thought (approximately 3:30 AM), that it is due to both accelerated glucose production and impaired glucose utilization, and that nocturnal increases in sympathetic nervous system activity and/or growth hormone secretion, but not changes in secretion of cortisol, adrenaline and glucagon or changes in insulin clearance, may be of pathogenetic importance.
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PMID:Sequence of events during development of the dawn phenomenon in insulin-dependent diabetes mellitus. 390 50

Forty-seven patients with insulin-dependent diabetes (IDDM) and diabetic nephropathy and 47 controls with IDDM without diabetic nephropathy were interviewed about their previous and current smoking habits. The patients in the two groups were matched according to sex, age, age at onset, and duration of diabetes. All patients in the nephropathy group had proteinuria and decreased glomerular filtration. None in the control group had ever had proteinuria as tested by dip stick. The total amount of smoking until date of interview was estimated for each individual and presented as an index. The patients with nephropathy had a significantly higher smoking index than the controls. In the nephropathy group there were also more numerous current smokers, more heavy smokers and fewer individuals who had never smoked than in the control group. The link between diabetic renal microangiopathy and smoking may be through mechanisms such as increased platelet aggregation, accentuated tissue hypoxia and hemodynamic or metabolic effects of repeated noradrenaline release.
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PMID:Smoking and diabetic nephropathy. 673 Oct 38

The antilipolytic effect of insulin in vitro was investigated in conditions known to be associated with resistance to the effect of insulin on glucose metabolism. Human subcutaneous adipose tissue was obtained from 14 obese subjects before and during starvation for 7 days, 12 untreated non-insulin dependent diabetics (NIDDM), 6 untreated insulin dependent diabetics (IDDM), and 10 nonobese control subjects. The tissue was incubated with and without insulin in concentration ranging from 1-10,000 microunits/ml. Responsiveness (maximum effect) and sensitivity to insulin were determined under basal induction conditions, since insulin had a bimodal effect on noradrenaline stimulated lipolysis. Under normal conditions both insulin sensitivity and insulin responsiveness were positively correlated with the basal rate of lipolysis. In obesity, IDDM and NIDDM there were no change in insulin sensitivity or in insulin responsiveness. When the obese subjects were divided into one hyperinsulinemic group (6 individuals) and one group with normal fasting serum insulin levels (7 individuals) a similar antilipolytic effect of insulin was observed in the two groups. During starvation there was a 20-fold increase in insulin sensitivity (p less than 0.01) but no change in insulin responsiveness in femoral fat and only a decrease in responsiveness (p less than 0.01) in abdominal fat. The present data supports the view that antilipolysis in human fat cells is not involved in the insulin resistance seen in obesity, starvation, diabetes and hyperinsulinemia.
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PMID:The antilipolytic effect of insulin in human adipose tissue in obesity, diabetes mellitus, hyperinsulinemia, and starvation. 702 6

A modified M-mode ultrasound echo system had been employed to study blood-vessel geometry of the intact femoral artery before and after Norepinephrine (NE) infusion. 14 patients with juvenile IDDM aged below 35 years and 11 healthy subjects participated in the study. In the diabetic group, wall distensibility (delta D/delta P) was reduced (p less than 0.01) at control conditions. After NE infusion, wall distensibility decreased in both groups (p less than 0.01). The decrease of wall distensibility is due to an increase in pulse pressure (delta P) (p less than 0.002) in the diabetic group and a reduction of pulsatile diameter (delta D) (p less than 0.02) in the normal group. Increased stiffening of the arteriaL wall after NE infusion with progressive reduction of wall strain (delta D/Dd) is the typical finding in the normal group. No change of wall strain was observed in the diabetic group. The functional alteration of the diabetic femoral artery may be described as diminished resistance of the arterial wall to the distending force of rising blood pressure.
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PMID:Influence of norepinephrine on vessel geometry of the intact femoral artery in juvenile insulin-dependent diabetics-evidence of early diabetic angiopathy in central arteries. 703 61


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