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)

1. Cataract formation in streptozotocin-induced diabetes in rats was reduced by approximately 85% when a diet rich in maize oil (300 g/kg diet) (fat diet) was given, thus confirming results of earlier studies. However, the concentration of sorbitol in the lens of diabetic animals remained high, the values for diabetic rats given the standard diet and the fat died being 65 and 40 mumol/g protein respectively. 2. With the standard diet, the fatty acid profile of the triglycerides of the epididymal fat pads was characterized by a greater relative proportion of saturated fatty acids for the diabetic animals compared to that for the normal animals. The fat diet moderated the tendency towards saturation in the diabetic animals. 3. The fat diet had other effects on the diabetic animals; these included a reduced mortality rate, increased body-weight, a decrease in the daily water intake, and in the daily urinary excretion of glucose and urea. 4. In the diabetic animals the fat diet had no effect on the specific activities in the liver of hexokinase (EC 2.7.1.1), glucokinase (EC 2.7.1.2), phosphofructokinase (EC 2.7.1.11) and pyruvate kinase (EC 2.7.1.40). However, the specific activity of glucose-6-phosphatase (EC 3.1.3.9) was reduced, while that of malate dehydrogenase (decarboxylating) (NADP) (EC 1.1.1.40) was increased. The NAD+:NADH ratio, as calculated from liver pyruvate and lactate concentrations, tended to increase. 5. The results suggested that the fat diet moderated the long-term metabolic effects of diabetes.
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PMID:The effect of an unsaturated-fat diet on cataract formation in streptozotocin-induced diabetic rats. 13 11

The articular cartilage of normal rats, of rats made diabetic with streptozotocin, and of rats made diabetic with streptozotocin and subsequently transplanted with isologous pancreatic islets was examined for the activities of enzymes engaged in the synthesis and degradation of glycosaminoglycans (mucopolysaccharides). The activities assayed were those of the degrading enzymes B-glucuronidase, B-acetyglucosaminidase, B-acetylgalactosaminidase, B-galactosidase, and those active in synthesis: uridine diphosphate dehydrogenase, glucose-6-phosphate dehyrogenase, and phosphofructokinase. In the diabetic animals all enzyme activities were increased, thos of the degrading enzymes more than those of the others. Implantation of pancreatic islets reversed the changes produced by diabetes, enzyme activities returning to near-normal levels.
Diabetes 1977 Aug
PMID:Enzyme studies in the articular cartilage of diabetic rats and of rats bearing transplanted pancreatic islets. 14 34

Acitivites of the hepatic enzymes were determined in spontaneous diabetes rats. The activities of the enzymes were compared with those in normal rats and in streptozotocin diabetic rats. In the spontaneous diabetes rats, glycogen phosphorylase and glycogen synthase were 14.6 +/- 0.6 and 1.73 +/- 0.15 U respectively. The activities of both the enzymes were significantly increased. In the spontaneous diabetes rats glucokinase was 3.82 +/- 0.5 U showing a significant increase. On the contrary, the activity of the enzyme was decreased in the streptozotocin diabetic rats. Glucose-6-phosphatase was increased both in the spontaneous diabetes rats and in the streptozotocin diabetic rats. Fructose-1,6-diphosphatase was increased in the spontaneous diabetes rats. Glucose-6-phosphate dehydrogenase was increased in the spontaneous diabetes rats and decreased in the streptozotocin diabetic rats. In the spontaneous diabetes rats phosphofructokinase showed a reduction of the activity and glucose-6-phosphate dehydrogenase was elevated. These findings are consistent with the results of activities of the hepatic enzymes in adult-onset diabetic patients. These patterns of the hepatic enzymes in the spontaneous diabetes rats were different from those in the streptozotocin diabetic rats. From these patterns of activities of the hepatic enzymes, the spontaneous diabetes rats produced by repetition of selective breeding according to Goto et al. (1975,1976) are an excellent model of human adult-onset diabetes.
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PMID:Activities of hepatic enzymes in spontaneous diabetes rats produced by selective breeding of normal Wistar rats. 15 47

The opinion is incorrect that the monofluor carbon-induced hyperglucosaemia which in literature is cited under the term fluor acetate diabetes is caused by insulin deficiency due to lesion of the pancreatic beta-cells. The cause of the fluor acetate diabetes is a disturbance of the glucose degradation by inhibition of the enzyme phosphofructokinase. Insulin applications have no causal influence on the monofluor carbon intoxications and no symptomatic influence on the fluor acetate diabetes.
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PMID:[What is fluoroacetate diabetes?]. 16 Jun 86

Hyperinsulinemia was produced in fetal rhesus monkeys for 21 days in the last third of gestation by subcutaneous pork insulin injected at 19 U a day. Plasma insulin concentrations in treated fetuses (N = 4) were 3525 microU/ml. There was no difference in paired pre- and post-treatment fetal plasma glucose concentration. Activity of the hepatic enzymes that promote glucose utilization (glucokinase and hexokinase) and glycolysis (phosphofructokinase, pyruvate kinase, and pyruvate dehydrogenase) was unaffected. Similarly, glycogen metabolism enzymes (active and inactive synthase and phosphorylase) were unaltered. Two gluconeogenic enzymes (PEPCK and glucose-6-phosphatase) were diminished in the treated group compared with controls. Fetal hyperinsulinemia enhanced lipogenic and NADPH-producing enzyme activities, as evidenced by a twofold increase in fatty acid synthase and in citrate cleavage enzyme activity. Malic enzyme was absent. Hyperinsulinemia with euglycemia (1) increases the activity of enzymes that participate in lipogenesis, (2) decreases some of those controlling gluconeogenesis, and (3) has no effect on the enzymes of glycolysis.
Diabetes 1979 Dec
PMID:Chronic hyperinsulinemia in the fetal rhesus monkey: effects on hepatic enzymes active in lipogenesis and carbohydrate metabolism. 22 50

Alloxan-induced diabetes of 4 days duration produced metabolite changes in brain compatible with severe reduction in cerebral metabolism (phosphocreatine increased 70%), and reduced phosphofructokinase activity (fructose diphosphate levels fell 38%). There was a 56% reduction in brain lactate concentration, but pyruvate levels were unchanged. In 5 of 23 animals, brain glycogen levels increased; in the remainder blycogen levels decreased. Brain fructose concentration, 0.4 mmol/kg, was only 1/30 of the glucose concentration. The alloxan-treated animals were also severely dehydrated. Therefore, to determine the casual relation of insulin deficiency to these findings, the effects of chronic dehydration and acute insulin deficiency were investigated. Findings in the brains of severely dehydrated animals (water deprivation and mannitol injections for 4 days) were almost identical with those seen after alloxan treatment. The exceptions were that, in the dehydrated mice, reductions in lactate and pyruvate were proportional, and glycogen levels were consistently reduced. In acute diabetes (6 to 24 hours after repeated anti-insulin serum injections) P-creatine, fructose diphosphate, and lactate levels were normal. Pyruvate levels were normal at 6 hours, but increased 39% by 12 to 24 hours; glycogen was 36% higher at 6 hours and 63% at 12 to 24 hours. Insulin (and glucose) appeared to be specific in correcting the metabolic abnormalities found in the brains of animals with alloxan-induced diabetes. At 4 and one half hours after treatment with insulin and glucose, glucose 6-phosphate levels fell 25%, fructose diphosphate increased 28%, and lactate and the lactate to pyruvate ratio returned to normal; glycogen increased 50%. However, the treatment also had a dramatic clinical effect. Since animals gained 8 to 27% of body weight during therapy, at least some of the improvements in metabolite levels could be related to rehydration.
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PMID:Effects of alloxan diabetes, anti-insulin serum diabetes, and non-diabetic dehydration on brain carbohydrate and energy metabolism in young mice. 111 28

Erythrocytes from young type I diabetic patients (n = 11), incubated in their plasma in anaerobic conditions, exhibited higher glucose consumption than cells from controls (n = 11). This increased metabolic activity is believed to reflect erythrocyte alterations dependent on the degree of metabolic control, as glucose consumption was significantly correlated to glycosylated haemoglobin (HbA1) and to glucose levels (P < 0.05 and P < 0.01 respectively). Red cell hexokinase (HK) and pyruvate kinase (PK) activities were similar in both groups whereas phosphofructokinase (PFK) activity was slightly higher in patients' cells (P < 0.05). No difference was found between patients and controls for red cell ATP and 2.3 diphosphoglycerate (2.3 DPG) levels. However, the concentrations of these glycolytic products seem also closely related to the glucose homeostasis in diabetes. Indeed, within the diabetic group, ATP levels showed a negative relationship with glucose level (P < 0.05) and 2.3 DPG a positive relationship with HbA1 (P < 0.05). In conclusion, higher glycolytic activity is present in young diabetic red cells. This activity as well as ATP and 2.3 DPG levels are related to the degree of short- or long-term diabetic control. These findings stress the importance of a careful metabolic control to avoid haematological disturbances.
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PMID:Erythrocyte metabolic alterations in type I diabetes: relationship to metabolic control. 144 91

This is a report investigating the methylglyoxal (MG) bypass in animals, by which D-lactate is produced from triosephosphate via MG. Rats were made diabetic using streptozotocin or starved for 72 h. D-Lactate and various metabolites related to it, such as L-lactate, pyruvate, methylglyoxal, glucose, and inorganic phosphate, were measured in the blood plasma, liver, and skeletal muscle of the rats. Diabetic and starved rats had significantly higher levels of D-lactate in plasma, liver, and skeletal muscle compared with the control group. In contrast, pyruvate levels in plasma, liver, and skeletal muscle was markedly lower than normal in diabetic and starved rats. L-Lactate level lowered markedly in plasma, liver, and skeletal muscle of starved rats and elevated in liver of diabetic rats. Differences between plasma L-lactate level for diabetes and control were not significant. MG level was significantly elevated in plasma and depressed in livers and muscles of starved rats as well as livers of diabetic rats. Hepatic glycerol content was markedly increased in those states. Enzyme activities related to D- and L-lactate, such as pyruvate kinase, phosphofructokinase, aldolase, and glyoxalase I, were measured in the livers of these rats. Pyruvate kinase activity decreased in these states, but other enzyme activities showed no significant changes. D-Lactate was much more excreted than L-lactate in the urine of diabetic and fasted rats compared with normal rats.
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PMID:Concentrations of D-lactate and its related metabolic intermediates in liver, blood, and muscle of diabetic and starved rats. 148 Aug 18

Phosphofructokinase activity was measured in the sciatic nerve of streptozotocin-induced diabetic and nondiabetic rats. Average steady-state phosphofructokinase activity was obtained from three consecutive segments of the mid-femoral region in the left sciatic nerve in both diabetic (4 and 24 weeks) and nondiabetic, age-matched animals. Over time, phosphofructokinase activity significantly decreased (p less than 0.05) with diabetes, with no effect demonstrated within similar age-groups. The accumulation of phosphofructokinase activity was accomplished by ligating the mid-femoral region of the right sciatic nerve for 24 h. Anterograde and retrograde axonal transport of phosphofructokinase was measured in the 3-mm segment proximal and distal to the ligature, respectively. There was a trend (p = 0.0627) towards a decline in net proximal accumulation (mean proximal minus mean background) with age. Net distal (mean distal minus mean background) activity declined by 80% (p less than 0.05) in the control group between 4 and 24 weeks of the diabetic state. However, diabetic animals did not experience the same age-related decline in retrograde transport. The findings suggest that diabetes affects the age-associated evolution of retrograde transport, presumably a reflection of the neuropathy occurring in the distal axon branches, without altering anterograde transport to any appreciable extent.
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PMID:Diabetes affects retrograde but not anterograde transport of sciatic nerve phosphofructokinase in Sprague-Dawley rats. 170 40

The fate of D-[2-3H] glucose and D-[5-3H] glucose in pancreatic islets was simulated in models with or without enzyme-to-enzyme tunnelling of hexose 6-phosphates in the glycolytic cascade. Satisfactory values for the recovery of phosphoglucoisomerase activity, for the ratio between unlabelled D-glucose 6-phosphate and D-fructose 6-phosphate, and for the time course of both 3HOH production from D-[2-3H] glucose and tritiated D-fructose 1,6-bisphosphate generation from D-[5-3H] glucose were only reached in models with enzyme-to-enzyme tunnelling, with emphasis on the coupling between phosphoglucoisomerase and phosphofructokinase.
Diabetes Res 1991 Jan
PMID:Hexose metabolism in pancreatic islets (time course of 3HOH production from tritiated D-glucose in models with and without enzyme-to-enzyme tunnelling). 181 93


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