PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ALLOXAN DIABETES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

[Lymphopoietic function of mice with alloxan diabetes].

Alloxan diabetes (sucrose blood concentration greater than or equal to 14 mmol/l) induced lymphocytopenia in noninbred male mice, resulting from the decrease in the number of both T and B lymphocytes differentiated by their reaction to acid phosphatase. At the same time thymic bone marrow lymphopoiesis in mice with diabetes was depressed. Nodular and splenic lymphopoiesis remained virtually unchanged. These disturbances became apparent on the 3rd week after diabetes induction. Alloxan itself has no inhibitory effect on lymphopoiesis.

Animals↗
PubMedDate not supplied

[Interrelation of the processes of lipid peroxidation and hydroxylation in the liver microsomal fraction of white rats with alloxan diabetes].

Alloxan diabetes was accompanied by an increase in ascorbate-NADPH-dependent lipid peroxidation with a simultaneous decrease in content of cytochrome P-450 and in the rate aniline hydroxylation in rat liver microsomal fraction. Activation of lipid peroxidation, which led to impairment of the endoplasmic reticulum integrity as well as to destruction of cytochrome P-450, may be important in pathogenesis of alloxan diabetes.

Animals↗
PubMed1990

[Kinetics of lymphocytes in mice with alloxan diabetes].

Alloxan diabetes (sucrose blood concentrate greater than or equal to 14 mmol/l decreased the life time of blood lymphocytes and increased the migration of these cells from lymphatic organs in BALB/c male mice. The proliferation pools of lymphoblasts and prolymphocytes in the thymus of diabetic mice were depressed, but in the lymphatic nodes remained unchanged. It has been shown that in lymphoid cells of the thymus of mice with diabetes the generation time and the time of G1- and G2-phase were significantly increased, but the time of the S-phase of the life cycle of these cells was normal. Proliferation of the lymphoid cells in lymphatic nodes was insulin-dependent. It has been shown that in the prolymphocytes of lymphatic nodes from diabetic mice the duration of the G1-phase was significantly decreased.

Animals↗
PubMedDate not supplied

[Effect of hydrocortisone on intensity of (3H)methionine incorporation into rat polyribosome and cytosol proteins in alloxan diabetes].

Alloxane diabetes decreases the intensity of [3H] methionine incorporation into total proteins of the liver cells polyribosomes and cytosol. Administration of hydrocortisone for seven days aggravate this disturbances and insulin injections level them. A combined administration of both hormones weakens the negative effect of hydrocortisone on the intensity of the amino acid incorporation and the glucose level in blood.

Animals↗
PubMedDate not supplied

[Normalizing effect of Bryonia alba L. on blood phospholipids in alloxan diabetes].

Alloxane diabetes in rats was accompanied by a distinct increase in total content of phospholipids and their fractions (especially of acid phospholipids) in whole blood; the ratio of neutral phospholipids/acid phospholipids was decreased. Content of phospholipids was distinctly normalized in rat blood after intramuscular administration of Bryonia alba extract into the diabetic animals at a dose of 0.5 mg/100 g of body mass.

Animals↗
PubMed1977

The prostatic lobes and the seminal vesicles in non-diabetic and alloxan-diabetic castrated adrenalectomized rats injected with cortisone.

The growth of the prostatic lobes and the seminal vesicles was studied morphologically in alloxan-diabetic and non-diabetic castrated adrenalectomized rats. In non-diabetic but not in alloxan-diabetic rats cortisone in daily doses of 3 or 6 mg induced growth and secretory activity in the epithelium of the dorsolateral prostate, the coagulating glands and the seminal vesicles. Insulin administration to alloxan-diabetic rats could restore the effect of cortisone on these glands. This indicates that insulin deficiency per se was the main reason for the failure of cortisone to induce secretory activity of the prostatic lobes and the seminal vesicles of alloxan-diabetic rats.

Adrenalectomy↗
PubMed1991

Thromboxane A2 receptor stimulation similarly potentiates pressor responses to 5-hydroxytryptamine in perfused hindquarters of non-diabetic and alloxan diabetic rats.

1. Dose-response curves were obtained to bolus injections of 5-hydroxytryptamine (5-HT) in Krebs'-perfused hindquarters of male Wistar rats. Vasoconstrictor responses to 5-HT (5.7-363 nmol/kg) were significantly attenuated in hindquarters of alloxan-treated 14 day diabetic rats compared with non-diabetics. 2. Infusion of the thromboxane A2 (TxA2)-mimetic U46619 (317 and 31.7, but not 3.17 nmol/L) significantly potentiated vasoconstrictor responses to 5-HT in Krebs'-perfused hindquarters of non-diabetic and diabetic rats. The degree of potentiation was similar for both groups. 3. In Krebs'-perfused hindquarters of non-diabetic rats, infusion of the alpha 1-adrenoceptor agonist methoxamine (8.96 mumol/L, which caused a rise in perfusion pressure intermediate in magnitude to that produced by infusion of 31.7 and 317 nmol/L U46619) did not significantly affect responses to bolus injections of 5-HT. 4. The same concentration of methoxamine did not cause a significant potentiation of vasoconstrictor responses to 5-HT (except for the two highest 5-HT doses, 182 and 363 nmol/kg) in hindquarters of diabetic rats. This potentiation was significantly less than that due to 317 nmol/L U46619, although there was no significant difference between the rise in basal perfusion pressures produced by these concentrations of methoxamine and U46619. 5. Infusion of the TxA2 receptor antagonist AH23848 (111 nmol/L) inhibited the potentiating effect of U46619 (317 nmol/L) on responses to 5-HT in both non-diabetic and diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

Temperature dependence of glucose transport in erythrocytes from normal and alloxan-diabetic rats.

Alloxan diabetes increased 3-O-methylglucose transport rates in rat red blood cells (RBC) at temperatures below 30 degrees C and decreased them above 30 degrees C. Preincubation of RBC from control rats with 20 mM glucose, 3-O-methylglucose, 2-deoxyglucose or xylose greatly elevated transport at 14 degrees C by increasing Vmax. The effect was slight at 40 degrees C. Preincubation with glucose or deoxyglucose alone caused a 50% depression of transport rates at 40 degrees C as a result of a rise in the Km, which is similar to findings in cells from alloxan-diabetic rats. Measurement of intracellular glucose metabolites suggested inhibition of glycolysis in cells from diabetic rats and a positive correlation between the level of intracellular hexose monophosphates and transport inhibition. Membrane fatty-acid and cholesterol composition and membrane lipid-ordering as monitored by electron paramagnetic resonance were not altered by alloxan diabetes. It is concluded that intracellular sugar and sugar metabolism alter the temperature dependence of glucose transport kinetics. Glucose metabolism can feed back to inhibit transport by increasing the transport Km at physiological temperatures only.

3-O-Methylglucose↗
PubMed1980

A quantitative comparison of motor and sensory conduction velocities in short- and long-term streptozotocin- and alloxan-diabetic rats.

Motor and sensory conduction velocities were measured in the sural and tibial nerves of streptozotocin (stz)-diabetic, alloxan-diabetic, and age-matched control rats. Conduction velocity (CV) determinations were made 2 weeks and 2, 4, 8, and 12 months following the induction of diabetes. CVs of control, stz-diabetic, and alloxan-diabetic rats were compared at each time period by one way analysis of variance and when appropriate by the Newman-Keuls multiple range test for multiple comparisons. Reductions of 10-20% in CV of diabetic rats were observed in several classes of sensory and motor nerve fibers. Larger reductions (31 and 38%) were seen in 2 classes of sensory nerve fibers in 12 month stz-diabetic rats. Sensory CV was slowed earlier and more frequently than motor CV. Differential involvement was also seen among the several classes of sensory nerve fibers examined. Slower conducting sensory fibers appeared to be affected earlier and more frequently than faster conducting sensory fibers. Comparing alloxan-diabetic with stz-diabetic rats revealed significant differences in CV 8 months after the induction of diabetes. Motor and sensory CVs of the tibial nerve were slower in stz-diabetic rats than in alloxan-diabetic rats. In general, the neuropathy appeared to be less severe and to develop later in the alloxan-diabetic rats. These data suggest that the neuropathy of stz- and alloxan-diabetes is primarily sensory in nature, and that the neuropathy in these 2 widely used models of diabetes may not be entirely equivalent.

Alloxan↗
PubMed1975

Potentiation of the hepatotoxic responses to chemicals in alloxan-diabetic rats.

Alloxan diabetes enhances the hepatotoxic response of male rats to chloroform and 1, 1, 2-trichloroethane, but not to trichloroethylene nor 1, 1, 1-trichloroethane. Insulin treatment partially protects the animals against the alloxan-induced enhancement of chloroform hepatotoxicity. Alloxan diabetes also enhances the hepatotoxic response to galactosamine but not to beryllium nor alpha-naphthylisothiocyanate.

1-Naphthylisothiocyanate↗
PubMed1950

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. III. The mechanism of the inhibition of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits.

A study of the serum lipids in normal and alloxan-diabetic rabbits during the course of cholesterol feeding is presented, particular attention being paid to the factors considered to be responsible for the stability of the serum lipids; namely, (1) their interrelations and (2) their association with the serum proteins. As far as the interrelations of the lipids were concerned a definite correlation was found between the development of atherosclerosis and an increase of serum cholesterol that was out of all proportion to the increase of serum lipid phosphorus and neutral fat. When these last two lipid constituents rose almost parallel with the serum cholesterol (as they did in some alloxan-diabetic rabbits), then the development of atherosclerosis was inhibited. This correlation was independent of the diabetic state, per se. It appeared likely that the marked elevation of serum neutral fat and lipid phosphorus in the diabetic animals was due to mobilization of body fat because of the disturbed carbohydrate metabolism. Because of their hydrophilic and emulsifying properties, it was thought probable that the elevation of the phospholipids was the important factor responsible for the stability of serum cholesterol. That neutral fat played a role, however, could not be denied. In normal rabbit sera, as we have previously shown, only small proportions of the lipid phosphorus and cholesterol are "readily extractable" (i.e., unattached or only loosely attached to protein). On the other hand, in every case in which the serum lipids were elevated, the greater proportion of the lipid phosphorus and cholesterol was "readily extractable," irrespective of whether atherosclerosis developed or was inhibited. Analysis of the lipid content of the aorta of rabbits not fed cholesterol, whether diabetic or non-diabetic, and from alloxan-diabetic rabbits fed cholesterol but protected from the development of atherosclerosis, showed that there was no significant difference in lipid content or composition among the animals of these groups. When atherosclerosis developed following cholesterol feeding, the lipid composition of the aortas was essentially the same in both control and diabetic animals. The deposited lipid consisted predominantly of cholesterol with small and fairly constant proportions of other lipids that did not vary significantly regardless of the quantities of these other lipids present in the circulating blood. In the less severe lesions the proportion of ester cholesterol was greater than that of free cholesterol, but in advanced lesions the reverse was true. The following conclusions are drawn concerning the pathogenesis of experimental cholesterol atherosclerosis in the rabbit: 1. Instability of cholesterol in the blood rather than hypercholesterolemia, per se, is the general condition responsible for the deposition of this substance in the arterial walls. 2. Of the two factors considered to be responsible for the stability of the lipids in the blood, the interrelations of the lipids appear to be more important than their relation to the serum proteins, at least in so far as the development of experimental cholesterol atherosclerosis is concerned. The importance of these conclusions in relation to the pathogenesis of human atherosclerosis is discussed.

Alloxan↗
PubMed1989

Changes in the activity of enzymes, participating in glycogen metabolism of alloxan diabetic rats.

Alloxan diabetes induced in white rats by intraperitoneal injection of alloxan-monohydrate (15 mg/100 g body weight) was used to study changes in the glycogen phosphorylase a and b, phosphoprotein phosphatases and hexokinase activities under insulin deficiency conditions. Among the enzymes studied, an increase in muscle phosphorylase a activity as well as the a/b ratio have been obtained. In diabetic muscle phosphoprotein phosphatases and hexokinase activities were diminished. AMP increased the liver glycogen phosphorylase activity twice in diabetic rats whereas in normal animals the enzyme was less sensitive to this effector. The changes in liver hexokinase activity at diabetes were not connected and correlated with the altered phosphorylase and protein phosphatase activities. The logical chain of probable molecular events taking place in muscle glycogen metabolism under the conditions of insulin deficiency is offered.

Animals↗
PubMed1975

Studies on gluconeogenesis, protein synthesis and cyclic AMP levels in isolated hepatocytes from alloxan diabetic rats.

Alloxan diabetic rats maintained on protamine zinc insulin for two weeks were used for these studies. Hepatocytes were isolated from these rats at various time intervals after withdrawal of insulin (0, 48, 72 and 96 hr). Gluconeogenesis with various concentrations of lactate and fructose was studied. Both lactate and fructose stimulated gluconeogenesis and showed progressive increases in glucose production up to 72 hr after the insulin withdrawal. Glucose production decreased at 96 hr. Protein synthesis in isolated hepatocytes from diabetic liver cells, as measured by the incorporation of radioactive isoleucine, valine and phenylalanine into protein, showed a decrease (5- to 6-fold) with time after insulin withdrawal. Glucagon (10(-6)M) alone increased cyclic AMP levels 10-fold in liver cells, in isolated cells from rats maintained on insulin (0 hr) or from rats withdrawn from insulin for 48 hr. The ability of glucagon to elevate cyclic AMP levels in isolated diabetic liver cells decreases 72 hr following insulin withdrawal.

Animals↗
PubMed1982

Effects of processed rye bran and raw rye bran on glucose metabolism in alloxan diabetic rats.

Alloxan diabetic rats (D) and control rats (C) were for 14 days fed a basic diet made from a mixture of rye bread and milk containing either no bran (group O), processed bran (group PB) or raw bran (group B). The D-B animals has a lower urinary glucose excretion (36 +/- 4 mmoles/24 hours) than the D-PB animals (63 +/- 5 mmoles/24 hours), which in their turn had a lower excretion than the D-0 animals (100 +/- 3 mmoles/24 hours). The effects of the two brans on weight, serum insulin levels, and non-fasting blood glucose levels were similar in D-rats as well as in C-rats, with the exception of the lower nonfasting blood glucose level in C-B animals than in C-PB animals.

Animals↗
PubMed1977

Impaired antibody responses in alloxan diabetic mice.

Alloxan diabetic BALB/C mice with high hyperglycaemia levels (larger than or equal to 600 mg/100 ml) when immunized either with T-dependent (SRCB) or T-independent (TNP-LPS) antigens show a significant decrease in the number of specific PFC when compared with normo-glycaemic controls. Moderate diabetes (greater than 350 mg/100 ml) does not affect the immune response and in some experiments a slight increase of anti-SRBC plaques was seen. In transfer experiments primed spleen cells of either diabetic or normal doners gave much better responses when transferred to normal rather than diabetic X-irradiated recipients. In Mishell-Dutton (MD) cultures anti-SRBC response of CBA spleen cells was moderately reduced only when the blood glucose level of cell donors exceeded 500 mg/100 ml. Glucose added to MD cultures of normal spleen cells diminished significantly the number of SFC when in concentrations exceeding 600 mg/100 ml. The data indicate that in diabetic animals B-lymphocyte function may be affected but give no clear-cut answer to whether this is also true for T-helper cells. Disabled lymphocytes, whatever population they represent, may partially recover when transferred into normo-insulinic milieu. It may be inferred that under conditions tested neither hyperglycaemia nor excess of corticosteroid accounted significantly for the impaired humoral responses in diabetic animals. These experiments imply, however, that in hypoinsulinaemia the lack of saturation of insulin receptors on the lymphocyte, and possibly also macrophage, membranes renders these cells functionally inactive presumably due to accumulation of cyclic AMP in the cell membrane.

Adrenalectomy↗