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

In experiments on the isolated superior cervical sympathetic ganglia of rats with alloxan diabetes rhythmic stimulation of preganglionic nerves was effected; summation presynaptic spikes and EPSPs of ganglionic neurons were registered. In rats with moderately severe alloxan diabetes progressive depression of rhythmic ganglion potentials was connected with suppression of the mediator emission to the impulse due to rapid exhaustion of its operational fraction. Rats with severe diabetes displayed also postsynaptic suppression of the ganglionic neurons. Dynamic characteristics of the transmitter turnover assessed on the basis of consideration of the successive patterns of posttetanic potentiation showed insignificant changes in the mediator output and a significant (by 38%) suppression of the mediator reserve per sec in comparison with control.
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PMID:[Mechanisms of inhibition of synaptic transmission in the sympathetic ganglia of rats with alloxan diabetes]. 21 35

In order to elucidate a possible relationship between (Na+ + K+)-activated ATPase and intestinal absorption of actively transported monosaccharides enzyme activity was measured in mucosal cells from alloxan diabetic rats. The general effect of increasing capacity of active, Na+-dependent transport processes in diabetes mellitus is associated with a significantly enhanced (Na+ +K+)-activated ATPase activity in mucosal homogenate from diabetic animals. To study the localization of these effects within the cell we isolated purified brush borders and their substructures. To enable a comparison to be made between preparation procedures of diabetic and control animals the fractions were controlled by electronmicroscopy and by measuring the sucrase activity. In the purified brush border fraction of alloxan treated rats there was no significant increase in (Na+ + K+)-activated ATPase activity. Based on these results we conclude that the (Na+ + K+)-activated ATPase in the basolateral membranes was increased in alloxan diabetes, and it seems very likely that this enzyme is involved in the regulation of Na+-dependent transport processes.
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PMID:[Effect of alloxan diabetes on (Na+ + K+)-activated ATPase in brush border membrane of the mucosal cell of rat small intestine]. 21 7

The loss of glucose regulation of glycogen synthase in perfused livers from diabetic rats was associated with a substantial reduction in synthase phosphatase activity. Treatment of diabetic rats with insulin alone resulted in total restoration of the glucose effect and synthase phosphatase activity, while simultaneous treatment with cycloheximide severely reduced the hormonal effect. Although treatment of normal rats with cycloheximide had no effect on glucose activation of synthase, it did result in severe depletion of liver glycogen, increased liver glycogen phosphorylase activity, and elevation of liver adenosine 3',5'-monophosphate (cyclic AMP), but without elevation of liver protein kinase activity. Simultaneous treatment of alloxan-diabetic rats with insulin and cycloheximide resulted in reduction of total liver glycogen, increased phosphorylase activity, a reduction in the ability of insulin to lower hepatic cyclic AMP, and a further reduction of protein kinase activity. In summary, the effect of insulin treatment of diabetic rats to restore glucose regulation of hepatic glycogen synthase probably involves synthesis of new protein, and the data remain consistent with the hypothesis that the defect may be due to a diabetes-related deficiency in a specific synthase phosphatase and/or alteration of the synthase molecule itself.
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PMID:Glucose activation of liver glycogen synthase. Insulin-mediated restoration of glucose effect in diabetic rats is blocked by protein synthesis inhibitor. 21 47

The somatotropichormone (STH) content was studied in the hypophysis and the peripheral blood of rats with alloxan diabetes; the corticosterone content was determined in their peripheral blood. The STH content in the peripheral blood and the hypophysis of these rats failed to differ from that in the control group, but the blood STH content rose considerably in the sick animals. Exclusion of the insular apparatus function was accompanied by the adrenal gland hypertrophy, which correlated with the rise of the blood corticosterone level. The data obtained indicated that the insular apparatus insufficiency induced by alloxan was accompanied by changes in the somatotropic function of the hypophysis and of glucocorticoid function of the adrenal glands.
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PMID:[Study of the somatotropic function of the pituitary gland and the glucocorticoid function of the adrenal glands in rats with alloxan diabetes]. 22 91

The effect of alloxan-diabetes, and of pharmacological doses of hydrocortisone administered to normal and diabetic rats, on carbamyl phosphate:glucose phosphotransferase and D-glucose-6-phosphate phosphohydrolase (EC 3.1.3.9) activities of isolated hepatic nuclei and microsomes were studied by assay at pH 7 in the absence and presence of deoxycholate. Hormonally related alterations both in activity levels and in the activation by the detergent (i.e. latency) of activities of the two cellular structural elements differed significantly. Most strikingly, (a) a 3--4-fold increase in the levels of activities of nuclei was seen in response either to diabetes or to hydrocortisone administered to normal rats whether or not detergent was added to preparations prior to assay; (b) the normally low degree of stimulation by detergent of activities of nuclei was unaltered in diabetes, and (c) administration of the glucocorticoid to diabetic rats decreased activity levels and increased their activation by detergent. Directly contrasting responses were noted with isolated microsomal preparations. Fundamental differences in the enzymes in these two organelle preparations are thus demonstrated. It appears that both synthetic and hydrolytic activities of this enzyme of nuclei may be manifest in the presence of requisite substrates, and that activities of this organelle may become increasingly prominent under certain hormonally perturbed conditions.
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PMID:Responses of nuclear glucose-6-phosphatase to diabetes and to hydrocortisone administered to normal and diabetic rats differ from those of the microsomal enzyme. 22 43

Rodents have been used by many investigators for studies of the effects that maternal diabetes during pregnancy may have on developing fetuses. In Wistar rats, the induction of mild chronic diabetes at the onset of pregnancy by alloxan or streptozotocin results in abnormalities of the nervous system and the heart, recognized in embryos at 11--13 days' gestation. Thus, early organogenesis is evidently affected in these embryos. With a method which enables rat embryos to be cultured in vitro in serum for the period of their early organogenesis, the growth and differentiation of embryos from normal and from diabetic rats can be observed in some detail. It is also possible to compare the effects of normal and of diabetic maternal serum on their development. The results reported here show that embryos from diabetic animals are more likely to be retarded or abnormal than those from non-diabetic animals when cultured in identical serum. The development of both types of embryo is more successful in diabetic than in non-diabetic serum, however, possibly because of the higher glucose content of diabetic serum. Cultures of fetal organs may also be used as test systems for the effects of diabetic maternal serum. Sacral vertebrae, some of which fail to ossify in fetuses from daibetic rats, are now being grown in media containing diabetic serum. It is planned to test the effects of insulin on these cultures.
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PMID:Culture in vitro as a means of analysing the effect of maternal diabetes on embryonic development in rats. 25 41

Hydroxyl radicals have been implicated in various forms of tissue injury ranging from radiation-induced cell death to alloxan-induced diabetes in animals. Although hydroxyl radicals can be readily generated in vitro, for example by the action of radiation or from the reaction of ferrous (FeII) ions with peroxides, they have not been observed directly in vivo. Their involvement in tissue damage has generally only been inferred from studies with so-called selective radical scavengers. In this paper the validity of such inferences will be briefly discussed in the light of current knowledge about the mechanisms and rates of reactions of hydroxyl radicals with biological compounds.
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PMID:Hydroxyl radicals and biological damage in vitro: what relevance in vivo? 25 61

We have studied the effects of alloxan-induced diabetes and subsequent insulin replacement on albumin and total hepatic protein synthesis. Diabetes resulted in a reduction to approximately 20% of normal in albumin synthesis relative to the rate of total protein synthesis in vivo and a reduction to 10% in the absolute rate of albumin secretion by perfused livers. In contrast, the synthesis of total secretory protein and retained hepatic protein was affected to a lesser extent by diabetes. Treatment of diabetic rats with insulin restored rates of albumin and total hepatic protein synthesis to normal levels. The molecular basis of these alterations in albumin synthesis was investigated by examining albumin mRNA levels in livers of normal, diabetic, and insulin-treated diabetic animals. The level of albumin mRNA, whether assayed by cell-free translation or by hybridization to a specific complementary DNA probe, was markedly decreased in livers of diabetic animals and was restored to normal by insulin treatment. These changes occurred in parallel with changes in the rates of albumin secretion observed in perfused liver, suggesting that albumin mRNA content is the primary factor responsible for altering rates of albumin synthesis under these conditions.
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PMID:Correlation of albumin production rates and albumin mRNA levels in livers of normal, diabetic, and insulin-treated diabetic rats. 28 8

Xanthine dehydrogenase activity was determined in blood serum of rats in which diabetes had been induced by alloxan administration. The results show that there is no statistical significance in the difference found for normal and diabetic rats. Alloxan produced an inhibition in the enzyme activity in animals in which a carbon tetrachloride hepatotoxicity had been induced.
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PMID:Serum xanthine dehydrogenase of carbon tetrachloride-induced hepatotoxicity in alloxan-diabetic rats. 29 57

The relationship of diabetes to salivary gland metabolism has been investigated by comparing the levels of alpha-amylase, sialic acid and total protein in the parotid and submandibular glands, plasma and kidneys of control and alloxan-diabetic rats. A significant decrease in alpha-amylase activity was found in both the parotid and submandibular glands of the diabetic rats by use of both a chemical and an electrophoretic assay. Plasma and kidney levels of the enzyme were not altered in the diabetic rats. Sialic acid levels were not affected by the alloxan-induced diabetes. Although the total protein concentration was significantly altered only in the kidneys of the alloxan-diabetic rats, the electrophoretic patterns of both the parotid and submandibular gland soluble proteins were markedly different between the control and alloxan-diabetic rats. The electrophoretic data indicate that protein metabolism in general, and the alpha-amylase concentration specifically, are altered in the salivary glands of alloxan-diabetic rats.
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PMID:Effect of alloxan-diabetes on alpha-amylase and sialic acid levels in the parotid and submandibular glands of rats. 30 11


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