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

Pretreatment with n-butanol (10 mmol/kg i.p.) 30 minutes before alloxan (100 mg/kg) protects mice from the permanent hyperglycemic effects (measured at 72 hours) of the diabetogenic agent. This dose of n-butanol caused an elevation of serum glucose at 30 minutes, the time of alloxan administration. Since glucose administration can protect animals from alloxan, the possibility that alcohol-induced hyperglycemia protected mice from alloxan was investigated. Mannoheptulose, an antagonist of glucose action at the pancreatic beta-cell, when given 24 minutes after n-butanol and 6 minutes before alloxan, eliminated the alcohol-induced protection. Fasted mice did not exhibit n-butanol-induced hyperglycemia at 30 minutes and alloxan given at that time produced diabetes. No protection was observed in fed animals when n-butanol was given 5 minutes before alloxan. The high serum levels of butanol and normal serum glucose which were observed at 5 minutes after alcohol administration indicated that the lack of protection was not due to a lack of circulating alcohol but resulted from an absence of hyperglycemia. The results indicate that pretreatment with n-butanol protects mice from alloxan-induced diabetes by the indirect mechanism of producing hyperglycemia at the time of alloxan administration.
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PMID:Mechanism of protection from alloxan diabetes provided by n-butanol. 32 64

The kariometric method was used to study the response of the nerve cells of the Nucl. dorsalis nervi vagi to insulin deficiency in rats with alloxan diabetes. Response to experimentally-induced diabetes of the nerve cells of the Nucl. tractus solitarii, adjacent nucleus in the medulla oblongata, served as control. In both cases the size of the cell nuclei of the areas under study was compared with the size of the cell nuclei in the same regions of the medulla oblongata of intact rats. Distinct and statistically significant shifts in the size of the cell nuclei of the Nucl. dorsalis nervi vagi in rats with alloxan diabetes were revealed in comparison with control measurements. Thus, sensitivity of the central nucleus of the vagus to insulin deficiency was revealed. Possible ways of participation of the vagus in the control of the insular apparatus are discussed.
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PMID:[Experimental aspects of the central nervous system - the insular system. 2. Reaction of the dorsal nucleus of the vagus nerve to insulin deficiency]. 32 70

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.
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PMID:Impaired antibody responses in alloxan diabetic mice. 33 63

Alloxan infused into the isolated perfused rat pancreas caused transient insulin secretion release. Alloxan poisoning also prevented subsequent induction of glucose-mediated unsulin release and also prevented the inhibition of glucagon release by glucose. Glucose or 3-O-methylglucose infused simultaneously with alloxan protected the alpha- and beta-cell, allowing subsequent glucose inhibition of glucagon secretion and stimulation of insulin release. The above alloxan effects were dose-related, the alpha-cell being one fourth as sensitive to alloxan as the beta-cell. The data indicate that (1) alloxan and glucose suppression of amino-acid-stimulated glucagon secretion is independent of concomitant insulin secretion; (2) alloxan, like glucose, affects alpha-and beta-cells directly, stimulating the beta-cell and inhibiting the alpha-cell; and (3) alloxan acts on a glucoreceptor system with comparable physicochemical characteristics common to both cell types.
Diabetes 1977 Oct
PMID:Glucose and 3-O-methylglucose protection against alloxan poisoning of pancreatic alpha and beta cells. 33 68

In hagfish islet parenchyma, consisting practically only of insulin-producing B-cells and agranular B-cell precursors, the contents of glutathione (GSH) and total protein-free thiols (NPSH) were determined on micro-dissected islet lobules. GSH was found to be of the same order of magnitude (22-25 mg/100 g wet weight) as in the islet parenchyma of a previously studied teleost fish and of some mammals, including man. However, the NPSH was found to be considerably higher in the islet lobules of the hagfish than in the teleostean islet parachyma. As in both teleost fish and mammals, GSH made up most of the NPSH in the hagfish erythrocytes, myocardium, and skeletal musculature. This discrepancy between hagfish islet parenchyma and other tissues indicates that the non-GSH portion of NPSH may be of particular significance for the insulin-producing B-cells. By means of flameless atomic absorption spectrophotometry the contents of zinc, cobalt, and manganese were determined in micro-dissected hagfish islet lobules. Neither zinc, nor cobalt, occurred in significantly higher concentrations in the islet parenchyma than in the liver or the skeletal musculature. Only manganese was found in somewhat higher amounts in the islet lobules than in the other tissues, but the contents were still low. The results indicate that none of the three heavy metals play any important role in the synthesis, storage, or release of insulin in the hagfish. The significance of this in relation to the prevailing hypotheses regarding the pathogenesis of alloxan diabetes is discussed.
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PMID:Microchemical assays of glutathione, zinc, cobalt and manganese in micro-dissected areas of the endocrine pancreas in the hagfish, Myxine glutinosa. 33 56

The preventive effect of ursodesoxycholic acid on pancreatic injury by alloxan (alloxan diabetes) has been reported by Watari, et al. (1976). In the following experiment, to pursue the findings further, ursodesoxycholic acid was used curatively for alloxan diabetes. A first group of animals (5 mice) were injected with alloxan (4 mg) twice at the fifth and tenth day. The second group (5 mice) was injected with ursodesoxycholic acid (0.2 mg each) for 14 days during the experiment in addition to the same alloxan dosage/frequency as the first group. A third group of animals (5 mice) served as the control. The animals were sacrificed on the 15th day and the blood sugar levels were examined, using commercial test paper. The pancreatic tissues were fixed in a mixture of 2.5% glutaraldehyde and 2% osmid acid solution, which was adjusted at pH 7.4 with a veronal acetate buffer; the osmotic pressure was also regulated by adding sucrose of 0.045 g/ml. Following dehydration using a series of alcohol concentrations, the tissues were embedded in Epon 812. Thin sections were cut with a Porter-Blum MT-2B ultramicrotome, stained with both uranyl acetate and a lead mixture, and then observed by electron microscopy. The results were as follows: The pancreatic islet cells, especially of B-cells in the first group of animals injected with alloxan only, were seriously damaged and contained myelinated mitochondria. Golgi apparatus, and an increasing number of autophagic vacuoles. Some B-cells revealed hydropic degeneration. Some B-granules changed into vacuoles after diacrine secretion. Pancreatic A-cells were increased in number and showed no cell injuries. On the other hand, the pancreatic B-cells of mice treated with both alloxan and ursodesoxycholic acid maintained almost normal fine structures. In summary, ursodesoxycholic acid has a curative effect on alloxan-induced pancreatic B-cell injury.
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PMID:[Electron microscopical observations on the curative effect of ursodesoxycholic acid in alloxan-induced pancreatic islet cell injury (author's transl)]. 33 78

The pancreatic insulin-, glucagon-, and somatostatin-positive cell populations were quantitated in normal and alloxan-diabetic rats. The method of quantitation (linear scanning) allowed an estimation of absolute changes in these cell populations through 14 months of diabetes. The changes in cell masses were correlated with changes in plasma and pancreatic immunoreactive insulin and glucagon. A marked reduction in the insulin-positive beta cells was demonstrated within seven days after alloxan treatment. No significant change in the glucagon-positive alpha cell population was noted in the diabetic rats when compared with normoglycemic controls. A statistically significant increase in the pancreatic somatostatin-positive delta cell population was demonstrable only after 14 months of alloxan diabetes. The results would suggest that the hyperglucagonemia of insulin-deficient diabetes is not a consequence of an increased pancreatic alpha cell population. In addition, since the increase in the pancreatic delta cell mass was found only late in the course of alloxan diabetes in the rat, the increase in delta cells is probably not of significance in the pathophysiology of diabetes in this experimental model.
Diabetes 1977 Dec
PMID:Morphometric quantitation of the pancreatic insulin-, glucagon-, and somatostatin-positive cell populations in normal and alloxan-diabetic rats. 33 4

Distribution and activity of acetylcholine esterase (AChE) in the central vagal nuclei (Nucl. dorsalis and Nucl. ambiguus) in male intact rats and in rats with experimental alloxan diabetes were investigated. In alloxan-diabetic rats there was noted an increase of the number of cells with a high AChE activity in the Nucl. dorsalis by 6%. These data suggest the participation of the vagal dorsal nucleus in the control of the endocrine function of the pancreas.
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PMID:[Sensitivity of the central nuclei of the vagus to insulin deficiency in rats (histoenzymologic study)]. 33 76

Isolated rat islets were maintained in a simple static incubation system and were exposed to alloxan for a period of five minutes. Alloxan inhibited subsequent glucose-induced insulin release in a dose-dependent manner at 37 degrees C., with 650 muM alloxan producing 94 per cent inhibition of insulin release. Barbituric acid, a compound structurally related to alloxan, provided complete protection (at 37 degrees C.) against this inhibition of insulin release when present during the alloxan exposure. At 23 degrees C., barbituric acid was shown to be absent from the intracellular space of the islet yet still protected completely against alloxan inhibition of insulin release. Thus, barbituric acid apparently provided protection against alloxan in the extracellular medium. By fluorometric and chromatographic analyses, it was determined that barbituric acid reacted rapidly with alloxan to produce a new compound. These findings indicate that barbituric acid protected against alloxan by a chemical reaction in the medium.
Diabetes 1978 Feb
PMID:Mechanism of barbituric-acid protection against inhibition by alloxan of glucose-induced insulin release. 34 21

Experiments were conducted on 250 albino female rats, 100 to 120 g in weight. A study was made of the influence of nerobol on the insular apparatus of the pancreas. A 10-day administration of nerobol in a dose of 10 mg/kg stimulated the functional activity of the insular apparatus, facilitated the course of alloxan diabetes, increased the tolerance of the beta-cells of the islets to alloxan both in intact and in castrated female rats.
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PMID:[Effect of nerobol on the histophysiology of the islands of Langerhans of intact and castrated female rats]. 34 63


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