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

The effect of short-term and long-term streptozotocin-induced diabetes on the pattern of distribution and tissue content of adrenergic and peptidergic nerves in ileum and distal (descending) colon of the rat was examined using immunohistochemical, biochemical, and immunochemical techniques. The effect of short-term streptozotocin-induced diabetes on the level of noradrenaline compared with weight-restricted (starved) and untreated controls in the celiac (celiac-superior mesenteric ganglia complex) and inferior mesenteric ganglia, which supply the two regions of the intestine, was also compared. The pattern of change in the distribution of dopamine-beta-hydroxylase-, substance P-, calcitonin gene-related peptide-, and vasoactive intestinal polypeptide-like immunoreactive nerve fibres that was observed in the ileum from diabetic rats was not evident in the myenteric plexus of distal colon. In contrast to the ileum, there was no evidence of degenerative change in any of the nerve types investigated in the myenteric plexus of the distal colon. The level of vasoactive intestinal polypeptide in the diabetic rat ileum was significantly increased, whereas the level of noradrenaline was reduced; no such changes were observed in the distal colon. The tissue content of noradrenaline in the celiac ganglion, which projects to the ileum, was increased at 8-week diabetes compared with both weight-restricted and untreated controls, whereas the diabetic state had no effect on the levels of noradrenaline of the inferior mesenteric ganglion, which projects to the distal colon. It is concluded that there is a differential effect of streptozotocin-diabetes on different regions of the rat intestine. The adrenergic and peptidergic innervation of the distal colon were changed little compared with ileum. This may be explainable in terms of the different functional roles of these two regions of the intestine and/or by the difference in origin of the sympathetic nerves supplying the two regions of the intestine.
 ...
PMID:Differential effect of streptozotocin-induced diabetes on the innervation of the ileum and distal colon. 200 99

The effects of procedures which stimulate sympathetic activity, viz. mental stress induced by a colour-word conflict test (CWT) for 20 min, and orthostasis (ORT) for 8 min were studied in 8 young (16-20 yr) insulin-dependent diabetes mellitus (IDDM) patients and 9 age and sex-matched healthy controls. The IDDM patients showed no signs of neuropathy or retinopathy and their mean HbA1c value was 8.4 +/- 0.6% (normal value less than 5.0%). Blood pressure and heart rate increased significantly during CWT and ORT in both groups. The changes in systolic blood pressure and heart rate were comparable in both groups during CWT; the IDDM group showed a higher (p less than 0.05) heart rate after 8 min of orthostasis, however. CWT and ORT elicited equivalent increases in noradrenaline in venous plasma in both groups (p less than 0.05), but the IDDM patients had 50% lower values (p less than 0.01) at rest, during CWT and at rest after CWT than controls. CWT and ORT evoked equivalent plasma adrenaline increases in both groups. The lipolysis marker, plasma glycerol, was about 40% lower (p less than 0.05) in the IDDM group before and after CWT. Yet, mental stress evoked equivalent increases in glycerol levels (p less than 0.01) in both groups. These findings indicate that sympathetic activity in the young diabetic patients without signs of neuropathy may be blunted.
 ...
PMID:Physiological effects of mental stress and orthostasis in young insulin-dependent diabetic patients. 202 92

The influence of metabolic control (HbA1c), noradrenaline (NA) and insulin-like growth factors (IGF-I and IGF-II) on renal function and size was investigated in 11 insulin-dependent diabetes mellitus patients aged 11-17 years. Renal function was evaluated in terms of glomerular filtration rate (GFR) and effective renal plasma flow (ERPF). Renal size was determined as renal parenchymal volume (RPV) by ultrasonography. The patients' HbA1c values ranged from 8.2% to 12.9% (normal range 5.5-8.5%) and their GFR and ERPF were higher than normal. Their IGF-II values were higher, and NA and IGF-I levels were lower than those of healthy controls. Inverse correlations between NA and GFR (r = -0.66) and NA and ERPF (r = -0.63) were found. No correlation was found between serum IGF-I and renal functional parameters. The IGF-II values correlated with GFR and HbA1c (r = 0.63, r = 0.70 respectively). There were linear correlations between RPV and GFR, RPV and ERPF, HbA1c and GFR, and ERPF and RPV. Decreased NA concentrations and increased IGF-II values appear to be factors contributing to renal hyperfunction in these patients.
 ...
PMID:Factors related to renal haemodynamics in young type-1 diabetes mellitus patients. 208 57

Neuropeptide Y (NPY) occurs within nerves in the rat pancreas, some of which are adrenergic. Therefore, we examined the influence of NPY alone and together with noradrenaline (NA) on insulin release in the rat. When infused alone for 30 min under basal conditions, NPY increased basal plasma insulin concentrations by 32 +/- 13 microU/ml at the highest dose level tested (68 pmol/min), as compared to +7 +/- 7 microU/ml in the controls (p less than 0.05). In contrast, NPY at 17 pmol/min reduced the plasma insulin response to both glucose (by 11%; p less than 0.001) and to arginine (by 26%; p less than 0.001). Infusion of NA alone (340 pmol/min) significantly elevated the basal plasma insulin levels by 41 +/- 4 microU/ml (p less than 0.001). NPY (17 pmol/min) completely abolished this effect (p less than 0.001). When NA (340 pmol/min) was added to an ongoing glucose infusion, the plasma insulin levels were markedly reduced (by 48%; p less than 0.001). By introducing NPY (17 pmol/min), this inhibitory action occurred more rapidly. However, NPY did not affect the maximal response to NA. In isolated rat islets, both NPY (10(-6) M) and NA (10(-6) M) inhibited glucose-stimulated insulin secretion. However, the maximal inhibitory effect exerted by the two neurotransmitters was not altered by giving them together. We conclude that, in the rat, NPY and NA both elevate basal plasma insulin levels and inhibit stimulated insulin secretion. In combination, NPY also induces a more rapid onset of the inhibitory action of NA on glucose-induced insulin secretion.
Diabetes Res 1990 Jan
PMID:Insulin secretion in rats: effects of neuropeptide Y and noradrenaline. 209 94

Diabetes-associated hypertension is accompanied by high levels of body sodium and cardiovascular hyper-reactivity to noradrenaline. Captopril, a promising drug for the treatment of hypertension in diabetics, may influence sodium metabolism and adrenergic pathways. This possibility was investigated in 11 patients with non-azotaemic diabetes mellitus and hypertension, studied after a 3-week placebo phase and after an 8-week phase of captopril treatment (50-100 mg/day). Blood pressure, exchangeable body sodium, blood volume, plasma renin activity, angiotensin II (Ang II), aldosterone, catecholamine levels and the pressor reactivity to infused Ang II or noradrenaline were measured. Compared with placebo, captopril caused a significant decrease in arterial pressure and stimulation of plasma renin activity. Exchangeable sodium, blood volume, plasma Ang II, aldosterone, noradrenaline and adrenaline levels, the pressor and aldosterone responsiveness to infused Ang II and the pressor response to infused noradrenaline (alone or combined with atropine) were not modified. These findings suggest that in hypertensive diabetics angiotensin converting enzyme inhibition causes a marked decrease in blood pressure. The mechanism of action is unrelated to changes in body sodium or noradrenergic-dependent pressor reactivity. In the stable phase of therapy, Ang II-dependent pathways are left unaltered when captopril is administered twice a day.
 ...
PMID:Cardiovascular regulation during angiotensin converting enzyme inhibition with captopril in diabetes-associated hypertension. 216 58

Plasma catecholamine levels, total platelet alpha 2-adrenoceptor number and affinity state (using [3H]-yohimbine binding) have been investigated in insulin-dependent diabetic patients with (n = 12) or without (n = 10) orthostatic hypotension as well as in normal control subjects (n = 6). Mean resting basal catecholamine values were similar in the three groups. One min standing elicited an increase in norepinephrine plasma level (but not in epinephrine plasma levels) in control group but not in diabetic patients (with or without orthostatic hypotension). The maximal number of platelet alpha 2-adrenoceptors (and Kd) calculated by [3H]-yohimbine saturation experiments was similar in the three groups. The percentage of platelet alpha 2-adrenoceptors in high affinity state determined by inhibition experiments of [3H]-yohimbine binding by UK14,304 (a specific alpha 2-adrenergic full agonist) was significantly lower in diabetic patients with orthostatic hypotension (29.2 +/- 5.3%) than in the other two groups. No significant difference was found between the control group (60.0 +/- 2.0%) and diabetic patients without orthostatic hypotension (64.3 +/- 3.1%). These results indicate that orthostatic hypotension in insulin-dependent diabetic patients is marked by a lack of noradrenaline increase in standing position and by a decrease in platelet alpha 2-adrenoceptors in high affinity state. Thus we suggest that orthostatic hypotension of diabetes mellitus is the result of sympathetic nerves injuries and of abnormalities in alpha 2-adrenoceptors coupling.
 ...
PMID:[Platelet alpha 2 adrenergic receptors, plasma catecholamines and orthostatic hypotension in insulin-dependent diabetic patients]. 217 83

After several years of insulin therapy, about 20% of insulin-dependent diabetics have little or no perception of hypoglycaemia because of a loss of the adrenergic warning symptoms. This defect, poorly correlated with the presence of autonomic neuropathy, has been classically explained by a defect in the catecholamine secretion. We compared the hormonal counterregulation during hypoglycaemia induced by subcutaneous injection of insulin in 7 insulin-dependent diabetics with poor perception of hypoglycaemia and experiencing repeated episodes of severe hypoglycaemia (group A) and 7 insulin-treated diabetics with very good perception of hypoglycaemia and not experiencing severe hypoglycaemia (group B). Groups A and B were similar in terms of age, duration of diabetes, HbA1c level and degenerative complications. The glucagon levels were identical and non-reactive in the two groups. The basal levels and secretion peaks of adrenaline, noradrenaline, growth hormone and cortisol were similar between the two groups, but there was a significant delay in secretion in group A with a blood glucose threshold of adrenergic secretion of between 3.1 +/- 0.5 and 1.6 +/- 0.2 mmoles/l in group A and between 4.6 +/- 0.3 and 3.2 +/- 0.2 mmoles/l in group B (P less than 0.05). This delayed secretion could be explained by desensitisation of the hypothalamic glucostat and could be due to the frequency and/or severity of hypoglycaemic episodes.
 ...
PMID:Unawareness of hypoglycemia by insulin-dependent diabetics. 218 5

To evaluate the renin-angiotensin-aldosterone system in relation to circulatory catecholamines, we determined renin activity, angiotensin II, aldosterone, adrenaline, and noradrenaline in plasma before and during a submaximal bicycle exercise test in 23 Type 1 (insulin-dependent) diabetic patients (aged 19-57 years, mean 37; duration of diabetes 2-32 years, mean 16), 17 with signs of cardiac autonomic neuropathy, and in 18 healthy non-diabetic subjects (aged 24-41 years, mean 29). At rest, Type 1 diabetic patients showed significantly lower aldosterone values than control subjects (0.14 +/- 0.02 nmol/l and 0.22 +/- 0.02 nmol/l; p less than 0.01) while renin activity (1.0 +/- 0.1 nmol.l-1.h-1 and 0.9 +/- 0.1 nmol.l-1.h-1) and angiotensin II (14 +/- 1 nmol/l and 18 +/- 2 nmol/l) did not differ significantly between patients and control subjects. During exercise, increments (increase from the resting value to the value at 80% of maximal working capacity) in renin (1.5 +/- 0.4 nmol.l-1.h-1 and 3.7 +/- 0.5 nmol.l-1.h-1; p less than 0.001), angiotensin II (28 +/- 8 nmol/l and 60 +/- 8 nmol/l; p less than 0.001), aldosterone (0.16 +/- 0.04 nmol/l and 0.25 +/- 0.05 nmol/l; p less than 0.05), adrenaline (1.96 +/- 0.49 nmol/l and 2.92 +/- 0.51 nmol/l; p less than 0.05), and noradrenaline (12.01 +/- 1.25 nmol/l and 18.74 +/- 1.45 nmol/l; p less than 0.01) were significantly lower in the patients than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The activity of the renin-angiotensin-aldosterone system before and during submaximal bicycle exercise in relation to circulatory catecholamines in patients with type 1 (insulin-dependent) diabetes mellitus. 207 87

A 61-year-old woman who presented with diabetes, nausea, weight loss and sweating was found to have a phaeochromocytoma secreting adrenaline, with a small amount of N-methyladrenaline. There was no significant increase in noradrenaline secretion. She was normotensive, and developed profound hypotension in response to the alpha-adrenergic antagonist phenoxybenzamine. These features are unusual in phaeochromocytoma, but similar features occurred in the very few previous reported cases of pure adrenaline-secreting phaeochromocytoma. We conclude that it is important to identify such patients, so that they should not be given alpha-adrenergic antagonist drugs.
 ...
PMID:A predominantly adrenaline-secreting phaeochromocytoma. 221 78

1. The role of protein kinase C (PKC) in mediating enhanced contractile responses of aortae and mesenteric arteries from male rats with 12-14 week streptozotocin-induced diabetes to noradrenaline (NA) was investigated using the PKC activator, phorbol 12,13-dibutyrate (PDB), and the PKC inhibitor, staurosporine. 2. Maximum contractile responses of aortae and mesenteric arteries from diabetic rats to NA were significantly enhanced compared with responses of arteries from age-matched control animals. The maximum NA responses were increased by 59.6 +/- 7.9% in aortae and by 54.9 +/- 7.4% in mesenteric arteries from diabetic animals, compared to their respective controls. 3. Pretreatment of aortae and mesenteric arteries from both control and diabetic animals with staurosporine (5 x 10(-8) M) caused marked inhibition of contractile responses to a maximum concentration of NA (10(-5) M in aortae; 3 x 10(-5) M in mesenteric arteries). In the presence of staurosporine, no difference was observed in the magnitude of contractile responses of arteries from control and diabetic rats to NA. 4. Maximum contractile responses of mesenteric arteries from diabetic rats to PDB were significantly increased (by 45.0 +/- 4.9%) compared to responses of arteries from control animals. In contrast, no significant difference was found in the magnitude of contractile responses or aortae from control and diabetic rats to PDB. 5. Staurosporine (5 x 10(-8) M caused marked attenuation of contractile responses of arteries from control and diabetic rats to a maximum concentration of PDB (3 x 10(-6) M). In the presence of staurosporine, the difference in magnitude of contractile responses of mesenteric arteries from control and diabetic rats to PDB was abolished. 6. Contractile responses of aortae and mesenteric arteries from control and diabetic rats to PDB were reduced in the absence of extracellular Ca2", and in the presence of the Ca2 + channel blockers, nifedipine (3 x 10-6 M) or verapamil (3 x 10-6 M). Under these conditions, no difference was found in the magnitude of contractile responses of mesenteric arteries from control and diabetic rats to PDB. 7. These data suggest that enhanced contractile responses of aortae and mesenteric arteries from streptozotocin-induced diabetic rats to NA may result, at least in part, from increased activation of PKC. In addition, increased activation of PKC-mediated processes, which are dependent on the presence of extracellular Ca2+, may further contribute to the enhanced contractile responses of diabetic mesenteric arteries to NA.
 ...
PMID:Protein kinase C-mediated contractile responses of arteries from diabetic rats. 225 45


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>