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


Diabetes 1979
PMID:Program. 39th Annual Meeting. American Diabetes Association. June 10--12, 1979. Los Angeles, California. Abstracts. 3 45

The metabolism of benzo[a]pyrene (BP) by microsomes from hepatic and extrahepatic tissues of female diabetic rats was investigated. Diabetes was produced by the administration of streptozotocin, 60 mg/kg iv, and BP metabolism was studied 7 or 10 days later. BP metabolism was increased in hepatic microsomes by 75% in diabetic animals. Cytochrome P-450 levels were similarly increased. BP mono-oxygenase activity was tripled in intestinal microsomes of diabetic rats, and returned to control values on insulin treatment. The BP mono-oxygenase activity in lung microsomes from diabetic rats decreased by 40%, and was increased to control levels after insulin treatment. No significant changes in BP metabolism were observed in the kidney and adrenal tissues of diabetic animals.
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PMID:Benzo[a]pyrene metabolism by hepatic and extrahepatic tissues in streptozotocin-diabetic rats. 3 27

In the presence of glucose (2 mg/ml), leucine (10 mM) noticeably increased islets' NADPH contents as well as the NADPH:NADP ratio; the changes occurred as soon as 1 min after its addition. NADH concentrations were also increased by leucine. The NADPH:NADP ratio as well as insulin release stimulated by glucose plus leucine were markedly decreased by methylene blue. The thiol oxidants diamide and tert-butyl hydroperoxide also inhibited insulin secretion in response to glucose plus leucine. Employing the perfused pancreas technique, the insulin-releasing action of p-chloromercuribenzoate was further enhanced by leucine. The combined effects were inhibited by tert-butyl hydroperoxide, however. Our data suggest that the insulin-releasing action of leucine depends on the islets' NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio. From the data, we assume that the observed increase of NADPH may lead via GSH to an increase in the number of such thiol groups in the beta-cell membrane, which are believed to be related to stimulation of insulin release and, thus, to increase the sensitivity of the beta-cell to stimulation by glucose and/or leucine.
Diabetes 1979 Jun
PMID:Effect of leucine on the pyridine nucleotide contents of islets and on the insulin released--interactions in vitro with methylene blue, thiol oxidants, and p-chloromercuribenzoate. 3 18


Diabetes 1979 Jul
PMID:Gastric and pancreatic release of somatostatin-like immunoreactivity during the gastric phase of a meal: effects of truncal vagotomy and atropine in the anesthetized dog. 3 19

Factors that influence hemoglobin (Hb)A(Ic) synthesis by intact erythrocytes were studied in vitro. After incubation cells were lysed, and hemoglobins were separated by isoelectric focusing on polyacrylamide slab gels and quantitated by microdensitometry. HbA(Ic) increased with time, glucose concentrations (5-500 mM), and incubation temperature (4 degrees -37 degrees C). Low temperatures allowed prolonged incubations with minimal hemolysis. At 4 degrees C HbA(Ic) increased linearly with time for 6 wk; after incubation at the highest glucose concentration, HbA(Ic) comprised 50% of total hemoglobin. Insulin (1 and 0.1 mU/ml) did not affect HbA(Ic) synthesis in vitro. In addition to glucose, galactose and mannose, but not fructose, served as precursors to HbA(Ic). A good substrate for hexokinase (2-deoxyglucose) and a poor hexokinase substrate (3-O-methylglucose), were better precursors for HbA(Ic) synthesis than glucose, suggesting that enzymatic phosphorylation of glucose is not required for HbA(Ic) synthesis. Autoradiography after erythrocyte incubation with (32)P-phosphate showed incorporation of radioactivity into HbA(Ia1) and A(Ia2), but not HbA(Ib), A(Ic), or A. Acetylated HbA, generated during incubation with acetylsalicylate, migrated anodal to HbA(Ic) and clearly separated from it. Erythrocytes from patients with insulinopenic diabetes mellitus synthesized HbA(Ic) at the same rate as controls when incubated with identical glucose concentrations. Likewise, the rate of HbA(Ic) synthesis by erythrocytes from patients with cystic fibrosis and congenital spherocytosis paralleled controls. When erythrocytes from cord blood and from HbC and sickle cell anemia patients were incubated with elevated concentrations of glucose, fetal Hb, HbC, and sickle Hb decreased, whereas hemoglobins focusing at isoelectric points near those expected for the corresponding glycosylated derivatives appeared in proportionately increased amounts.
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PMID:Synthesis of hemoglobin Aic and related minor hemoglobin by erythrocytes. In vitro study of regulation. 3 12

The activity of enzymes with a regulatory function in the pathways of glycolysis, gluconeogenesis, NADPH generation and fatty acid synthesis was measured in the placenta and liver of rats. Compared with the liver, a high activity of pyruvate kinase was found in the placenta, indicating a high glycolytic potential; a small capacity for gluconeogenesis was also present and a moderate to low activity of enzymes associated with lipogenesis. The activity of all placental enzymes fell from day 15 to 20 of gestation irrespective of the pathway they represented. The pattern of decline continued when the gestation was prolonged up to day 26 by the administration of chorionic gonadotropin. The rates of activity disappearance over 11 days of gestation differed for each enzyme, with half-lives ranging from 2.7 days for NADP-malate dehydrogenase to 7 days for glucose-6-phosphate dehydrogenase. In contrast, the activity of hepatic enzymes either remained unchanged or showed individual adaptation to the advancing pregnancy. The regression in placental metabolic capacity after day 15 of gestation was also evident by the decrease in glucose uptake and its channelling to lactate, CO2, glycerol and fatty acids. In addition, placental ageing was associated with triglyceride accumulation, mainly due to the decrease in free fatty acid oxidation. Treatment of pregnant rats with several hormones, while markedly affecting the hepatic enzyme activities, failed to induce appreciable changes in the corresponding placental enzymes. This was illustrated in the case of triiodothyronine treatment. Similarly, insulin deficiency induced by streptozotocin failed to elicit adaptive changes in placental enzyme activities typical of diabetes like those occurring in the maternal liver; some converse responses in the placenta were attributed to hyperglycaemia. On the other hand, responses in some fetal liver enzymes were suggestive of fetal hyperinsulinaemia. These observations indicate that placental enzymes are not susceptible to endocrine regulation and imply that placental metabolism is largely independent of the physiopathological alterations affecting the maternal organism. The gradual activity decreases with gestation suggest that the enzyme complement of the placenta, once developed, is designed to last through its limited lifespan without continuous replenishment. Within this context, no mechanism seems to operate to ind1ce the adaptive synthesis of individual enzymes, and the age of the placenta appears to be the primary factor determining its enzyme activity and metabolic performance.
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PMID:Regulation of placental enzymes of the carbohydrate and lipid metabolic pathways. 3 55

Glycemia, growth hormone level and urinary catecholamine excretion were studied in 182 patients suffering from insulin-dependent diabetes mellitus during insulin therapy alone, and in 33 during treatment with insulin plus alpha- and beta-adrenoblockers. Under the effect of alpha-adrenoblockers glycemia proved to fall in the insulin-dependent patients, without increasing the insulin dose. The STH level diminished in these patients under the effect of alpha-adrenoblockers, even when glycemia persisted at the same level. But beta-adrenoblockers aggravated decompensation and the STH level remained unchanged. alpha and beta-adrenoblockers decreased the urinary adrenaline excretion and elevated noradrenaline, dophamine and DOPA excretion, irrespective of blood glycemia. The authors recommend the use of alpha-adrenoblockers to prevent the necessity of a considerable elevation of insulin doses during compensation in patients with the insulin-resistant form of diabetes mellitus. beta-adrenoblockers are not recommended in diabetes mellitus.
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PMID:[Effect of alpha and beta receptor blockaders on the degree of glycemia, growth hormone content of blood and catecholamine excretion in insulin-dependent diabetes mellitus]. 3 98

A reversible deterioration of the oral glucose tolerance has been reported in subjects with initially impaired glucose tolerance when starting to take oral diuretics. This does not seem to be the case in subjects with an initially unimpaired glucose tolerance. A deterioration in the diabetic state is commonly seen when diuretics are given to subjects with clinical diabetes. Our knowledge about the effect of beta-blockers on the glucose tolerance is limited. As for diuretics there seems to be an overrepresentation of diabetics among subjects taking beta-blockers. This overrepresentation can probably be explained by an association between diabetes and disturbances in which diuretics and beta-blockers are commonly used such as arterial hypertension and ischaemic heart disease.
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PMID:Impairment of glucose metabolism during treatment with antihypertensive drugs. 3 6

12 heel necroses were seen in a group of 596 geriatric patients. The patients average age was 73 years. 3 tentative causes for the development of heel necrosis were investigated. 1. Imobility, 2. Arterial occlusive disease, and 3. Diabetes. Immobility was demonstrable in all cases. Additionally, arterial occlusions of the leg were present in 7 and diabetes in 6 patients. The percentage of arterial occlusion and diabetes was significantly higher in the heel necrosis group than in the overall hospital cohort. The two diseases can be looked upon as risk factors for the development of heel necrosis.
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PMID:[Heel necrosis: a complication of geriatric diseases (author's transl)]. 3 65

The effects of streptozotocin-induced diabetes and of starvation on the lysyl oxidase activity of rat lung were investigated. Enzyme activity was elevated 2--3 fold in the lungs of streptozotocin-diabetic rats. In contrast, starvation of rats produced a rapid loss of lung lysyl oxidase activity, with levels approximating 25% of control values after 48--72 h of starvation. Enzyme activity was essentially fully restored to control values upon refeeding the 48-h starved animals for 3 h. These studies demonstrate the responsiveness of lysyl oxidase to these physiological states and suggest a component, enzymatic basis of change in lung function known to occur in the diabetic state.
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PMID:Changes in lung lysyl oxidase activity in streptozotocin-diabetes and in starvation. 3 20


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