Studies on the Mechanism of Alloxan Diabetes

Goldner, Martin G.; Gömöri, George

doi:10.1210/endo-35-4-241

Cited by 68 publications

(26 citation statements)

References 0 publications

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“…The alloxan is thus considered to affect the plasma membrane of B cells and the limiting membrane of B granules, and the hormonal substances are believed to be released through these membranes. This unusual increase of insulin released from the damaged cells is believed, as is generally accepted since the early works of RIDOUT, HAM andWRENSHALL (1944) andGOLDNER andGOMORI (1944) …”

Section: Alteration Of the Islet After Injection Of Alloxanmentioning

confidence: 68%

Some Observations on the Fine Structure of the Pancreatic Islet of Rabbits, with Special Reference to B Cell Alteration in the Hypoglycemic State Induced by Alloxan Treatment

Fujita

Matsuno

1967

Arch. Histol. Jap., Arch. Histol. Jpn

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Section: Alteration Of the Islet After Injection Of Alloxanmentioning

confidence: 68%

Some Observations on the Fine Structure of the Pancreatic Islet of Rabbits, with Special Reference to B Cell Alteration in the Hypoglycemic State Induced by Alloxan Treatment

Fujita

Matsuno

1967

Arch. Histol. Jap., Arch. Histol. Jpn

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“…Alloxan is a specific toxin that destroys the pancreatic ␤-cells, provoking a state of primary deficiency of insulin without affecting other islet types [30,31]. Diabetic effect of alloxan is due to excess production of reactive oxygen species (ROS) leading to toxicity in pancreatic cells which reduces the synthesis and the release of insulin [32] while affecting organs such as liver and pancreas [33].…”

Section: Discussionmentioning

confidence: 99%

Oral administration of levan polysaccharide reduces the alloxan-induced oxidative stress in rats

Dahech¹,

Belghith²,

Hamden

et al. 2011

International Journal of Biological Macromolecules

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“…1), is remarkably similar to that observed after the intravenous administration of alloxan (12). Since the early hyperglycemia which follows alloxan has been attributed to an adrenaline response (13), it is reasonable to consider a similar explanation for streptozotocin, although this interpretation has not as yet been tested experimentally. The hypoglycemic phase has been attributed, in the case of alloxan, to the release of insulin from necrotizing pancreatic P-cells, although elevated serum insulin levels have been reported only very recently (14,15).…”

Section: Methodsmentioning

confidence: 99%

Diabetogenic action of streptozotocin: relationship of dose to metabolic response

Junod¹,

Lambert²,

Stauffacher³

et al. 1969

J. Clin. Invest.

852

488

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A B S T R A C T The relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. Diabetogenic activity could be demonstrated between the doses of 25 and 100 mg/kg, all indices used showing some degree of correlation with the dose administered. Ketonuria was only seen with the largest dose, 100 mg/kg. The most striking and precise correlation was that between the dose and the pancreatic IRI content 24 hr after administration of the drug, and it is suggested that this represents a convenient test system either for both related and unrelated beta cytotoxic compounds or for screening for modifying agents or antidiabetic substances of a novel type. Ability to produce graded depletion of pancreatic IRI storage capacity led to an analysis of the relationship between pancreatic IRI content and deranged carbohydrate metabolism. Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached twothirds and three-quarters, respectively. The mild yet persistent anomaly produced by the lowest effective streptozotocin dose, 25 mg/kg, exhibits characteristics resembling the state of chemical diabetes in humans and might thus warrant further study as a possible model. Finally, the loss of the diabetogenic action of streptozotocin by pretreatment with nicotinamide was confirmed and was shown to be a function of the relative doses of nicotinamide and streptozotocin and of the interval between injections.

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Studies on the Mechanism of Alloxan Diabetes

Cited by 68 publications

References 0 publications

Some Observations on the Fine Structure of the Pancreatic Islet of Rabbits, with Special Reference to B Cell Alteration in the Hypoglycemic State Induced by Alloxan Treatment

Some Observations on the Fine Structure of the Pancreatic Islet of Rabbits, with Special Reference to B Cell Alteration in the Hypoglycemic State Induced by Alloxan Treatment

Oral administration of levan polysaccharide reduces the alloxan-induced oxidative stress in rats

Diabetogenic action of streptozotocin: relationship of dose to metabolic response

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