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

Accumulation of acetylcholinesterase (AChE) and choline acetylase (ChAc) activities proximal to a tie placed on the sciatic nerve was measured in control, untreated diabetic, and insulin-treated diabetic rats. In the diabetic animals AChE accumulation was reduced by about 20% and ChAc accumulation by about 40%. Insulin treatment eliminated the impairment. It remains an open question whether these reversible functional changes in rat have any counterpart in the diabetic neuropathy of man.
Diabetes 1975 Dec
PMID:Fast and slow axoplasmic flow in sciatic nerve of diabetic rats. 5 67

Quantitative radiometric assays were employed to measure activities of choline acetyltransferase and acetylcholinesterase in freeze-dried pieces of islets of Langerhans and exocrine tissue from rat pancreas. The activities of both enzymes were about an order of magnitude higher in islets than in exocrine tissue. This difference in activity was found in rats made diabetic with streptozotocin as well as in the controls. Although the enzyme activities in islets from diabetic rats averaged about 30-40% higher than those in islets from control rats, the differences were statistically only marginally significant. Since the islets of diabetic rats are probably much smaller than those of control rats, it is suggested that cholinergic elements associated with pancreatic islets are lost following induction of streptozotocin diabetes.
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PMID:Enzymes of the cholinergic system in islets of Langerhans. 12 56

This study examined the effects of myo-inositol treatment on the deficits of motor nerve conduction velocity and of axonal transport of choline acetyltransferase in rats with streptozotocin-induced diabetes. Motor nerve conduction velocity was measured in seven groups of male rats. Two groups formed nondiabetic controls; one survived for 3 and the other for 6 weeks, then motor nerve conduction velocity was again measured and the accumulation of choline acetyltransferase activity proximal to a 24-h sciatic nerve constriction was estimated. The other five groups were rendered diabetic and subjected to similar measurements. Two diabetic groups were untreated and survived 3 or 6 weeks. The other three groups received myo-inositol for 1, 2, and 3 weeks, respectively, commencing 21 days after induction of diabetes. These groups survived for 4, 5, or 6 weeks, respectively. In all groups surviving for longer than 3 weeks an interim measurement of motor nerve conduction velocity was made 21 days after the start of the experiment (immediately before onset of treatment in the treated groups). In these groups a third measurement was made on the day before death. At death, choline acetyltransferase accumulation was measured and the remainder of the sciatic nerves was assayed for sorbitol and myo-inositol. In the two untreated diabetic groups we found reduced motor nerve conduction velocity, a deficit in the accumulation of choline acetyltransferase proximal to the sciatic nerve constriction, and a marked build-up of nerve sorbitol and a depletion of nerve myo-inositol. All three treated groups showed a reversal of this myo-inositol depletion without a reduction in the nerve sorbitol content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversal of deficits in axonal transport and nerve conduction velocity by treatment of streptozotocin-diabetic rats with myo-inositol. 241 Feb 89

This investigation examined the effect of treatment of streptozocin-diabetic rats with the aldose reductase inhibitor "Statil" (25 mg/kg/day p.o.) on axonal transport in cholinergic neurons of the sciatic and vagal nerves and on nerve polyol and sugar levels. Three weeks of experimental diabetes caused deficits in the accumulation of choline acetyltransferase activity proximal to 24-h constrictions in the left sciatic and vagus nerves. These deficits did not develop in age-matched, similarly diabetic rats that were treated with the aldose reductase inhibitor. The inhibitor prevented completely the build-up of sorbitol and markedly reduced the build-up of fructose in the sciatic nerves of the treated diabetic rats. The inhibitor also prevented the depletion of myo-inositol that was seen in the untreated diabetic animals. It is suggested that these findings indicate a possible approach to the elucidation of the pathogenesis of cardiac vagal dysfunction in diabetes mellitus.
Diabetes 1985 Oct
PMID:Prevention of defective axonal transport in streptozocin-diabetic rats by treatment with "Statil" (ICI 128436), an aldose reductase inhibitor. 241 18

Concentrations of monoamines and their metabolites as well as the activities of tyrosine hydroxylase (TH) and of choline acetyltransferase were investigated in various brain regions of control and streptozotocin-treated Sprague-Dawley rats. The animals were rendered diabetic by a single i.v. injection of streptozotocin (65 mg/kg) and killed 10, 30 and 90 days after the treatment. During the course of diabetes, progressive decreases in the activity of TH and a marked increase in the concentration of norepinephrine were observed in several brain regions, including thalamus, hypothalamus, medulla and midbrain. This inverse relationship between TH activity and norepinephrine content was also seen in the pons but only in the 90-day diabetic animals. Lower TH activity in the hypothalamus of 30-day diabetic rats reflected a decreased Vmax, but no difference in the Km. The number of alpha adrenergic receptors was increased significantly in the hypothalamus, medulla and midbrain of the 30-day diabetic rats. The concentrations of dopamine and serotonin in various brain regions of the 10- and 30-day diabetic rats were generally not significantly different from controls. Concentrations of the acidic metabolites of these neurotransmitters, dihydroxyphenylacetic acid and 5-hydroxyindolacetic acid, were, however, greatly reduced. The activity of choline acetyltransferase, a marker of presynaptic cholinergic neuron activity, remained unaltered during the course of diabetes. These data suggest that uncontrolled diabetes is associated with a significant disturbance of brain monoamine metabolism.
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PMID:Diabetes-induced alteration in brain monoamine metabolism in rats. 241 97

Deficits of axonal transport in short-term experimental diabetes may be a consequence of increased sorbitol pathway flux and may contribute to the development of degenerative neuropathies. Therefore, we studied the effect of the aldose reductase inhibitor sorbinil on the axonal transport of choline acetyltransferase (ChAT) in the cholinergic neurons of the sciatic nerve of rats with short-term streptozotocin diabetes. In addition, to examine the extent of axonal transport deficits, we studied the axonal transport of choline containing lipids in sensory neurons of the sciatic nerve of similarly diabetic rats and the effects of sorbinil thereon. In experimentally diabetic animals, sorbinil both prevented and reversed deficits of the axonal transport of ChAT and prevented a deficit in the axonal transport of choline containing lipids.
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PMID:Studies of sorbinil on axonal transport in streptozotocin-diabetic rats. 242 Nov 36

This study determined the axonal transport of choline acetyltransferase (ChAT) activity and its content in several tissues in nondiabetic control rats and in four groups of rats with streptozotocin-induced diabetes of 6-months duration. Diabetic rats were either untreated, treated only with either the aldose reductase inhibitor Statil (Imperial Chemical Industries, Pharmaceuticals Division, Macclesfield, UK) or insulin, or were given the two in combination. Insulin treatment consisted of a single weekly injection of a long-acting insulin, a regime designed not to control the diabetes, but to provide regular respite from the catabolic dominance of uncontrolled diabetes. Elevated levels of sugars and polyols in the sciatic nerves of untreated diabetic animals were markedly attenuated by Statil. The reduced myo-inositol content and reduced axonal transport of ChAT activity also seen in these nerves were prevented by Statil, but a reduced motor nerve conduction velocity was attenuated only by Statil and insulin in combination. The presence of cataracts in all diabetic animals was associated with hyperhydration of the lens. The level of hydration and presence of cataracts were reduced by Statil, particularly in combination with insulin. ChAT activities of the iris, adrenal gland, and superior cervical ganglion were similar in all groups. Skeletal muscles showed wasting while the ileum showed an increased weight per unit length in diabetic rats. These tissues also displayed alterations in ChAT activities, particularly when referenced to unit weight of tissue, which may have been a consequence of the weight changes rather than diabetes per se.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on peripheral nerve and lens in long-term experimental diabetes: effects of the aldose reductase inhibitor statil. 245 59

Experiments were designed to gain information on the mechanisms leading to diabetic urinary bladder dysfunction. Bladders from control rats, animals subjected to 4-5 wk streptozocin-induced diabetes, and rats subjected to equivalent diuresis produced by 5% sucrose feeding were studied with an in vitro whole-bladder preparation and neurochemical measurements. The diuretic group was used to distinguish alterations produced by metabolic effects on nerve and muscle from those induced by prolonged periods of excessive diuresis. Diuresis alone explains many of the diabetes-induced effects, including decreased norepinephrine levels, postsynaptic supersensitivity for sympathetic regulation of bladder storage, decreased responsiveness to parasympathetic regulation of emptying, and enhanced prostaglandin F2 alpha-induced contraction. Other diabetes-induced effects were not observed in the diuretic controls and are presumed to result from metabolic alterations associated with diabetes. These effects were decreases in norepinephrine uptake and in choline acetyltransferase activity, both markers of nerve terminal function. Thus, diuretic and metabolic factors appear to contribute to the early signs of parasympathetic and sympathetic neuropathy. In contrast, we found no evidence for loss of sensory nerve function in the diabetic bladder, at least at the organ level, because no diabetes- or diuresis-induced changes were observed in responsiveness to substance P or capsaicin.
Diabetes 1989 Mar
PMID:Effects of diabetes and diuresis on contraction and relaxation mechanisms in rat urinary bladder. 256 11

The concentrations of acetylcholine (ACh) as a parasympathetic marker and norepinephrine (NE) as a sympathetic marker were investigated in the hearts of rats 2, 4, and 8 wk after the induction of diabetes by an injection of streptozocin (STZ; 65 mg/kg i.v.). ACh and NE were measured by high-performance liquid chromatography with electrochemical detection. Diabetic rats showed low body weight and heart weight at 2, 4, and 8 wk and higher heart-to-body weight ratio and bradycardia at 8 wk, almost all of which were normalized after insulin treatment. Myocardial ACh and NE concentrations in the diabetic rats at 2 and 4 wk were not significantly different from those in age-matched control rats. However, ACh and NE concentrations in the diabetic rats at 8 wk significantly increased compared with the control rats. Diabetic rats at 8 wk also had increased myocardial choline concentration and choline acetyltransferase activity and decreased acetylcholinesterase activity. Insulin treatment normalized all of these changes in the diabetic rats. Thus, in STZ-induced diabetes (STZ-D), the concentrations of both cholinergic and noradrenergic neurotransmitters in the myocardium increased. The results of this study confirm a previously reported increase in sympathetic activity to the heart and also indicate that there is an increase in the synthesis and a decrease in the metabolism of ACh in STZ-D and that adequate insulin treatment normalizes these changes.
Diabetes 1989 Feb
PMID:Altered acetylcholine and norepinephrine concentrations in diabetic rat hearts. Role of parasympathetic nervous system in diabetic cardiomyopathy. 264 43

The combined influence of diabetes and moderate treadmill exercise training on select metabolic and cardiovascular parameters was investigated with mature male Sprague-Dawley rats assigned to either control diabetic or diabetic groups receiving exogenous insulin. Experimental diabetes was induced with streptozotocin (80 mg.kg-1, i.v.) and verified by blood glucose concentrations greater than 16 mmol. The animals were designated as control, insulin-injected (5 U.kg-1, twice daily), or saline-injected (twice daily), and assigned to either non-trained or trained sub-groups. Insulin treatment partially restored the measured physiological functions to within normal limits. All animals were trained at 60 to 70% maximal oxygen consumption for 9 wk and exhibited higher maximal oxygen consumption values and cytochrome oxidase activity of the soleus muscles. Diabetes caused lower (P less than 0.05) reductions in resting heart rate but training-induced bradycardia did not occur in any group. Heart rate response to atropine sulfate (1 mg.kg-1, atrial choline acetyltransferase activity, atrial acetylcholine concentration, and quinuclidinyl benzilate binding was measured to evaluate changes in the parasympathetic nervous system. Atropine-induced cardiac acceleration was most pronounced in control and least effective in diabetic animals. Endurance training had no meaningful influence on this response to cholinergic inhibition. Quinuclidinyl benzilate binding for the diabetic and the diabetic groups receiving insulin revealed no change in receptor number, receptor affinity, or training effects. These findings indicated that 9 wk of exercise training improves the aerobic capability of insulin-deficient rats without changing cardiovascular characteristics associated with the parasympathetic nervous system.
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PMID:Select cardiovascular and metabolic responses of diabetic rats to moderate exercise training. 331 5


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