Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular disease in diabetics could arise in part from altered vessel wall catebolism. Specific activities of hydrolases in aortic smooth muscle cells from rats with streptozotocin-induced diabetes were measured. Enyzmes included: neutral alpha-glucosidase, alpha-mannosidase, and lysosomal N-acetyl beta-glucosaminidase, beta-galactosidase, cathepsin C, acid alpha-glucosidase, and acid cholesteryl esterase. After 4,8, and 11 weeks of diabetes, activities of all enzymes studied were decreased significantly in diabetic vessels, decreases ranging from 15% for cathepsin C to 62% for alpha-mannosidase. After 3 weeks of diabetes, insulin treatment for 1 week restored enzyme levels to normal. After 7 weeks of diabetes, 1 week of insulin treatment did not restore enzyme levels fully to normal (acid cholesteryl esterase was unchanged); 4 weeks of insulin did. Acid phosphatase and N-acetyl beta-glucosaminidase activities were reduced markedly in histochemical studies of diabetic aortas at all time periods and were restored by insulin treatment. Alloxan-induced diabetes gave results similar to those with streptozotocin. Significant decreases of aortic hydrolase activities, including those of lysosomes, occur in experimental diabetes mellitus and could contribute to accumulation of substrates in vascular smooth muscle cells.
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PMID:Hydrolase activities in the rat aorta. I. Effects of diabetes mellitus and insulin treatment. 14 80

Brush border sucrase and lactase activities are significantly elevated in alloxan-induced chronic diabetes and are restored to control levels after insulin treatment. Alkaline phosphatase and Mg-ATPase levels remain unchanged in diabetes, compared to a control group. Insulin treatment alone to control animals also led to enhanced activities of these enzymes.
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PMID:Effect of chronic alloxan diabetes and insulin administration on intestinal brush border enzymes. 14 19

A case of N-3 pyridylmethyl-N' 4 nitrophenyl urea (Vacor) rodenticide poisoning in a 52-year-old man is presented. Vacor is structurally related to alloxan and streptozotocin, agents that have been used extensively to produce diabetes mellitus in laboratory animals. Seven days after ingestion of Vacor, the patient presented in diabetic ketoacidosis complicated by postural hypotension and adynamic ileus. The patient recovered from ketoacidosis but has continued to require insulin. With infusion of arginine, glucagon rose from 185 to 650 pg./ml. and C-peptide from 0.5 to 3.4 ng./ml. Six weeks after onset of diabetes, no anti-islet-cell antibodies were detected. Muscle capillary basement membrane thickness on electron microscopy was found to be 1,918 +/- 194 A. The absence of hyperglycemia after Vacor ingestion should not lead to complacency on the part of the attending physician. The patient must be observed closely for development of ketoacidosis and treated prophylactically with nicotinamide, the suggested antidote.
Diabetes Care
PMID:Diabetes mellitus and autonomic dysfunction after vacor rodenticide ingestion. 15 23

Changes in immunoreactive somatostatin were examined in islets, whole pancreas, stomach, and hypothalamus of streptozotocin-diabetic rats. There was no change in islet somatostatin content at 2 days after the administration of streptozotocin, but thereafter, somatostatin progressively increased in the diabetic animals by 45% at 2 weeks, 230% at 6 weeks, and 500% by 6 months. By contrast, islet glucagon rose acutely and maintained a constant 2-fold elevation irrespective of the duration of the diabetes. Morphometric analysis of the somatostatin- and glucagon-producing cells in the islets revealed an apparent augmentation of both cell types. The concentration of somatostatin per total pancreas was also increased in the diabetic animals, suggesting that the islet increase was part of a true increase in pancreatic somatostatin. Pancreatic glucagon was unchanged despite the islet increase. The increase in pancreatic somatostatin was paralleled by an elevation in gastric somatostatin concentration, implying a common mechanism in response to streptozotocin for the somatostatin cells in these two sites. There was no change in hypothalamic somatostatin concentration. Islet somatostatin was also increased in alloxan-diabetic rats. suggesting that streptozotocin does not stimulate the D cells directly.
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PMID:Changes in somatostatin concentration in pancreas and other tissues of streptozotocin diabetic rats. 15 2

In order to study the modifications in the activity on some CNS drugs by the experimental diabetes, the authors are proposing a model of alloxanic diabetes in the mouse. Diabetes is induced by administering pure alloxan to a well selected brand of mice. Biochemical and histological observations obtained on different vital organs are comparable with those obtained with spontaneously diabetic mice (stable and steady glycemia). This model is consequently a good way of assessing pharmacological comparison.
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PMID:[Histologic aspects of some organs in the alloxan induced diabetic mouse]. 16 Aug 15

In alloxan-diabetic rats the protein level in the secomucoid and the levels of neutral sugars and peptides in the serum and urinary non-diffusible sugar-peptide (serum and urinary NSP) fractions increased. The proportion of neutral sugars in seromucoid and serum NSP fraction decreased, while in the urinary NSP fraction this ratio increased. In streptozotocin-diabetic rats the ratio of neutral sugars to the peptides did not change in either fraction, while the ratio of these sugars to the total nitrogen in the serum and urinary NSP fractions increased. The total level of seromucoid as well as the levels of neutral sugars in the serum and urinary NSP fraction were raised in these rats. The comparison of the results with those obtained previously by Sarnecka-Keller et al. (1968, 1972, 1972 a) in natural diabetes showed that the alloxan-diabetic model is more suitable for the study of glycopeptide compound metabolism in this disease.
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PMID:The influence of experimental diabetes on the serum and urinary glycopeptide compounds in rats. 16 75

Studies were performed to examine the effects of alloxan- or streptozotocin-induced diabetes on carbon tetrachloride (CCl4) liver injury. Male rats were pretreated with single i.v. injections of alloxan monohydrate (40 or 80 mg/kg) or streptozotocin (65 mg/kg). A challenging dose of CCl4 (0.1 ml/kg i.p.) was given to rats 4 days after alloxan pretreatment or 5 days after streptozotocin pretreatment, and the animals were sacrificed 24 hours later. Biochemical and morphologic evidence was obtained to show that pretreatment with the diabetogenic agents markedly enhanced CCl4-induced hepatotoxity. The challenging dose of CCl4 had no effect on the serum glutamic pyruvic transaminase (SGPT) activity in control rats. However, the administration of this dose of CCl4 to rats pretreated with 40 and 80 mg/kg of alloxan as well as to rats pretreated with streptozotocin resulted in 11-, 68-, and 32-fold increases, respectively, in SGPT activity. Hepatic triglyceride concentrations in the diabetic rats were also markedly elevated above control values after CCl4 challenge. Alloxan- or streptozotocin-pretreatment alone did not enhance these biochemical parameters of liver injury. Hepatic glucose-6-phosphatase activity, which increased in the rats given a diabetogenic agent, was lowered as a result of CCl4 injection. Insulin treatment of rats given alloxan (80 mg/kg) markedly protected against CCl4-induced hepatotoxicity. The severity of the morphologic changes in diabetic rats given CCl4 correlated with the biochemical findings.
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PMID:Potentiation of carbon tetrachloride-induced hepatotoxicity in alloxan- or strepto- zotocin-diabetic rats. 16 33

Experiments were conducted on rats. A study was made of the adrenal gland ACTH reactivity under conditions of alloxan diabetes. The function of the adrenal gland increased one month after the administration of alloxan; this was indicated by an increase of their absolute and relative weight, by an elevation of the corticosterone content in the peripheral blood and the glands proper. ACTH stimulated the adrenal gland function in rats with an intact pancreas, increasing the weight of the adrenal glands, the level of corticosterones in the blood and the adrenal glands. ACTH reactivity proved to be lowered in rats with alloxan diabetes. The blood corticosterone level increased in them less and changes in the weight of the glands and of the hormone concentration in them proved to be statistically insignificant.
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PMID:[Reactivity of the adrenals to ACTH in rats with alloxan diabetes]. 16 71

Intestinal absorption of L-histidine as affected by insulin, diabetes, hydrocortisone, adrenocorticotrophic hormone (ACTH) and thyroxine has been studied. Intestinal absorption of L-histidine is not significantly increased following insulin administration. Similarly, addition of insulin in vitro did not change the transport activity significantly. When rats are made diabetic on administration of alloxan monohydrate, the transport activity is increased. Hydrocortisone, adrenocorticotrophic hormone and thyroxine treatment increased the absorption of L-histidine by small intestine. However, addition in vitro of ACTH and hydrocortisone did not change the absorption of L-histidines by small intestine. It appears that the facilitative action of these hormones is not due to their direct action of the membrane.
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PMID:Studies on the action of hormones on the intestinal transport of L-histidine. 16

Gluconeogenic conditions, such as administration of triamcinolone or alloxan diabetes, cause the following changes in the molecular structure and properties of rabbit liver fructose 1,6-bisphosphatase (D-fructose-1,6-bisphosphate 1-phosphohydrolase, EC 3.1.3.11): (1) the appearance of traces (about 10%) of a lighter subunit; (2) loss of tryptophan from all of the subunits, including those that show no apparent change in molecular weight; (3) increase in requirement for the positive allosteric effector, histidine; (4) increase in amount of enzyme, but not its specific activity. These changes are identical to those induced by cold or fasting, and are related to increased activities of lysosomal proteases. The results suggest that lysosomes may act as mediators of gluconeogenic stimuli.
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PMID:Hormonal effects on structure and catalytic properties of fructose 1,6-bisphosphatase. 17 48


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