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)

The effect of hyperglycemia due to experimental diabetes induced in rats, causes a decrease in the activity of Acetylcholinesterase in brain regions and heart; changes in the heart being more significant than the brain. Insulin administration reversed this effect in both the hear and the brain. Significant increase in the levels of catecholamines were also found in the brain regions in diabetes, which was reversed by insulin. The decreased activity of acetylcholinesterase observed in diabetes may be due to an early impaired glucose oxidation and glucose transport as a result of lack of insulin, which causes specific alterations in neurotransmitter levels, thereby effecting blood brain barrier transport, thus causing brain dysfunction.
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PMID:Effect of hyperglycemia on acetylcholinesterase and catecholamine levels in rat brain and heart. 185 30

Insulin release is influenced by the autonomic nervous system. Regarding parasympathetic control, previous reports have shown that regulation of insulin release is executed exclusively through muscarinic receptors in the pancreatic islets. In the present study, however, we examined the effect on insulin release at the islet level of various agents affecting the parasympathetic nervous system, especially nicotinic receptor blockers. Pancreatic islets isolated from adult Wistar male rats were incubated with these agents and insulin release in the media was measured. Acetylcholine chloride (10(-5) M), as well as distigmine bromide (10(-6), 10(-5) M), both of which are cholinesterase inhibitors, stimulated insulin release, whereas atropine (5 x 10(-6), 5 x 10(-5) M) suppressed it. On the other hand, serum and IgG from myasthenia gravis patients, containing anti-acetylcholine receptor antibodies, affected insulin release, and alpha-bungarotoxin (10(-9)-10(-7) M), a nicotinic receptor blocker, stimulated insulin release dose-dependently. The present observations suggest that insulin release is influenced by the parasympathetic nervous system, mediated via not only muscarinic but also nicotinic receptors.
Diabetes Res Clin Pract 1990 Mar
PMID:Possible involvement of cholinergic nicotinic receptor in insulin release from isolated rat islets. 197 Dec 10

An histochemical research on cholinergic and noradrenergic fibres of the adventitia layer and of the myenteric plexus of the terminal ileum from rats with streptozotocin-induced diabetes, after 20 weeks of evolution of the illness, was carried out to study changes in the innervation of the gut. The cholinergic nerves, revealed through their acetylcholinesterase activity, did not present alterations, but an evident reduction in number of the noradrenergic nerves and swollen intensely fluorescent varicosities, were observed, both in the perivascular and myenteric plexus of terminal ileum from diabetic animals.
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PMID:Effects of experimental diabetes in the noradrenergic and cholinergic nerves of the rat small intestine. 213 72

Despite the fact that the significance of red cell membrane acetylcholinesterase (AChE) is unknown, this enzyme of red cell assumes importance since many of its properties have been found to be similar to purified enzyme form of brain tissues. Our investigations on the effect of insulin-dependent diabetes mellitus on red cell AChE revealed that the activity of this enzyme is significantly decreased in diabetes. Insulin treatment restored the activity to the normal level. Solubilization of normal, diabetic and insulin treated diabetic red cell membranes with Triton X-100 (0.2% v/v) caused a general decline in AChE activity, however the per cent decline in activity of diabetic enzyme was lower as compared to normal and insulin treated conditions. From our results it is inferred that the decreased red cell AChE activity in diabetes is due to lesser number of active enzyme molecules and also due to altered membrane microenvironment.
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PMID:Regulation of red cell acetylcholinesterase activity in diabetes mellitus. 219 39

In the present study we investigated the effects of the acetylcholinesterase inhibitor pyridostigmine (PD), which is hypothesized to decrease hypothalamic somatostatin tone, alone and in association with GH-releasing hormone (GHRH) on GH secretion in 18 type 1 diabetic patients and 12 normal subjects using a randomized double blind placebo-controlled protocol. All subjects received either 120 mg oral PD or placebo 60 min before iv injection of either human GHRH-(1-29) NH2 (100 micrograms) or sterile water (2 mL). In normal subjects both PD alone and GHRH alone caused a significant increase in GH. PD and GHRH acted in a synergistic fashion when combined. In diabetic patients the GH response to GHRH was variable. To segregate the responses, the ratio between the GH increase after GHRH plus PD and after GHRH alone was calculated for each subject. In 10 diabetic patients (group A) the ratio was lower than 2 SD (P less than 0.05) from the mean response of normal subjects. These patients showed an exaggerated GH increase after GHRH and a lower GH increase after PD with respect to normal subjects. Eight diabetic patients (group B) showed a ratio similar to that in normal subjects and similar GH responses to the stimuli. No significant differences were found between groups A and B with respect to age, body mass index, and blood glucose levels. Duration of diabetes was longer and basal GH levels were higher in group A. Hemoglobin-A1c was higher in group A, but of only borderline statistical significance (P = 0.052). Our data demonstrate that in diabetic patients with exaggerated GH responses to GHRH an increase in cholinergic tone does not affect GH secretion. These data suggest that in some type 1 diabetic patients an altered somatostatinergic control of GH secretion may contribute to their abnormal GH response to GHRH.
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PMID:Impaired growth hormone (GH) response to pyridostigmine in type 1 diabetic patients with exaggerated GH-releasing hormone-stimulated GH secretion. 222 5

RT6 is an unusual cell membrane protein that is expressed exclusively by postthymic T cells. The inherent defect in its expression has been correlated to lymphopenia and genetically determined susceptibility for insulin-dependent diabetes mellitus in the rat. We report here the primary structure of the RT6.2 alloantigen as deduced from the cDNA sequence. The predicted amino acid sequence of RT6.2 begins with a conventional leader of 20 amino acids and ends in a hydrophobic C-terminal extension peptide of 29 amino acids as is common for phosphatidylinositol-anchored proteins. Native RT6.2 is predicted to comprise 226 amino acids, with a calculated Mr of 26,036. Four cysteine residues account for two intrachain disulfide bonds. The sequence lacks potential N-glycosylation sites and contains an excess of positively charged residues. Homology searches in protein sequence data banks suggest that RT6.2 is not encoded by a member of the immunoglobulin supergene family. Moreover, these analyses did not reveal any close homologies of RT6.2 to known proteins: the highest homology found was 21.2% identity in a 52-amino acid overlap to the torpedo acetylcholinesterase precursor. Southern blot analyses indicate that RT6.2 is the product of a single-copy gene and provide evidence for closely related genes in the mouse and other species. The corresponding gene products remain to be identified.
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PMID:Primary structure of rat RT6.2, a nonglycosylated phosphatidylinositol-linked surface marker of postthymic T cells. 230 May 88

Longitudinal muscles from the ileum of rats rendered diabetic for 10 to 12 weeks by injection of streptozotocin (STZ) developed greater contractile force in response to muscarinic agonists, (acetylcholine, carbamylcholine and bethanechol) than muscles from age-matched control rats. There was no change, however, in the sensitivity of longitudinal smooth muscles to muscarinic agonists as reflected by the EC50 values for stimulation of muscle contraction. This increased responsiveness of the muscles was accompanied by a 32% reduction in the density of muscarinic receptors (381 +/- 93 vs. 560 +/- 74 fmol/mg of membrane protein) in muscles from STZ-diabetic rats. There was no change in agonist or antagonist binding affinities in muscles from diabetic rats, and there was no alteration in the distribution of receptors between the states characterized by high and low affinity agonist binding. There was also no change in acetylcholinesterase activity in muscle membranes isolated from STZ-diabetic rats. The origin of the increased responsiveness of ileal smooth muscles in this model of diabetes is not clear, but may involve changes in the muscarinic signal transduction pathway beyond the receptor level, or in the contractile apparatus itself.
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PMID:Increased muscarinic responsiveness and decreased muscarinic receptor content in ileal smooth muscle in diabetes. 238 82

The anterograde and retrograde axonal flow of acetylcholinesterase were studied in the sciatic nerve of alloxan-diabetic rats after five weeks of experimental diabetes. A slight reduction of the anterograde axonal flow of the enzyme was found in alloxan-diabetic compared to control rats. Sedimentation analysis revealed a major reduction of anterograde axonal flow of the light globular forms of the enzyme (G1 + G2), which are probably conveyed by slow transport. There was also a minor reduction of the anterograde flow of the globular form G4, while no modification of the axonal flow of the heavy asymmetric form A12 was found. Both G4 and A12 molecular forms are conveyed by fast axonal transport. In contrast, no abnormality of the retrograde axonal flow of acetylcholinesterase was observed. Ganglioside treatment antagonized the decline of the anterograde axonal flow of the enzyme in alloxan-diabetic rats. These results are consistent with the view that experimental diabetic neuropathy is associated with axonal transport defects, and suggest a protective effect of ganglioside treatment against neuronal damage(s) related to the diabetic syndrome.
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PMID:Impaired axonal transport of acetylcholinesterase in the sciatic nerve of alloxan-diabetic rats: effect of ganglioside treatment. 242 5

Penile tissue (consisting of corpus cavernosum and tunica albuginea) was obtained from 19 patients undergoing surgery for the implantation of penile prostheses. The tissue was examined for vasoactive intestinal polypeptide-like immunoreactivity in nerves, acetylcholinesterase-positive staining in nerves and noradrenaline content. Impotence was due to a variety of causes; 11 patients were classified as a 'non-neuropathic' group on the basis of their clinical history which included Peyronie's disease, vascular disease, hypertension and psychogenic impotence. Vasoactive intestinal polypeptide-like immunoreactive and acetylcholinesterase-positive nerves were present and the pattern and distribution were similar in each patient in this group. The noradrenaline content of the tunica albuginea was significantly lower than the corpus cavernosum (p less than 0.02), although there was a linear relationship between the noradrenaline contents of the two regions (r = 0.95, p less than 0.01). By comparison, a complete absence of vasoactive intestinal polypeptide-like immunoreactivity in nerves was observed in a patient with a cauda equina lesion. Five out of six diabetic patients studied revealed a marked reduction in vasoactive intestinal polypeptide-like immunoreactivity in nerves associated with the cavernous smooth muscle, while acetylcholinesterase-positive staining was reduced in three out of five diabetic patients studied. The noradrenaline content of the corpus cavernosum from diabetic patients was significantly lower (p less than 0.02) than that of the 'non-neuropathic' group. The noradrenaline content of the tunica albuginea, however, was similar in both groups. The results provide evidence that VIPergic, cholinergic and adrenergic nerves in the penis are affected in diabetes mellitus and thus may contribute to the development of impotence in diabetic patients.
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PMID:Changes in the VIPergic, cholinergic and adrenergic innervation of human penile tissue in diabetic and non-diabetic impotent males. 243 29

The gross anatomy and autonomic innervation of the ventral prostate glands was examined in control and streptozotocin-induced diabetic rats. The most striking finding was the consistent reduction in size and the gross atrophy of the prostates from diabetic rats. No change was detected in the total content of noradrenaline in the alveolar lobes or in the levels of vasoactive intestinal polypeptide, neuropeptide Y and substance P in the whole prostates of diabetic rats. However, histochemical and immunohistochemical investigations revealed localized reductions in density and/or fluorescence intensity of noradrenaline-containing nerve fibres and increased density and/or fluorescence intensity of vasoactive intestinal polypeptide- and neuropeptide Y-containing nerve fibres in the alveolar smooth muscle of a majority of diabetic animals. No changes in acetylcholinesterase-staining nerve fibres were seen. The adrenergic component of the autonomic nervous system in this gland appears to be particularly susceptible to change in diabetes.
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PMID:Histochemical and biochemical investigation of adrenergic, cholinergic and peptidergic innervation of the rat ventral prostate 8 weeks after streptozotocin-induced diabetes. 244 38


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